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Validated All-in-One™ qPCR Primer for PTGS2(NM_000963.3) Search again
Product ID:
HQP107759
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
COX-2, COX2, GRIPGHS, PGG/HS, PGHS-2, PHS-2, hCox-2
Gene Description:
prostaglandin-endoperoxide synthase 2
Target Gene Accession:
NM_000963.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
Prostaglandin-endoperoxide synthase (PTGS), also known as cyclooxygenase, is the key enzyme in prostaglandin biosynthesis, and acts both as a dioxygenase and as a peroxidase. There are two isozymes of PTGS: a constitutive PTGS1 and an inducible PTGS2, which differ in their regulation of expression and tissue distribution. This gene encodes the inducible isozyme. It is regulated by specific stimulatory events, suggesting that it is responsible for the prostanoid biosynthesis involved in inflammation and mitogenesis. [provided by RefSeq].
Gene References into function
- Increased expression of iNOS and production of prostanoids in colon cancer parallels the increase in COX-2, confirming the importance of this enzyme in colon cancer.
- Findings collectively suggest the possibility that COX-2 is mainly produced in follicles in a preovulatory phase, while after ovulation, COX-2 is produced in interstitial cells in human ovary.
- Cyclooxygenase-1 is up-regulated in cervical carcinomas: autocrine/paracrine regulation of cyclooxygenase-2, prostaglandin e receptors, and angiogenic factors by cyclooxygenase-1.
- induction in monocytes by peroxisome proliferator activated receptor gamma and oxidized alkyl phospholipids from oxidized low density lipoprotein
- increased expression associated with chemotherapy resistance and poor survival in cervical cancer
- Up-regulation of prostaglandin E2 synthesis by interleukin-1beta in human orbital fibroblasts involves coordinate induction of prostaglandin-endoperoxide H synthase-2 and glutathione-dependent prostaglandin E2 synthase expression
- Aromatase and COX-2 expression in human breast cancers.
- Inhibition of cyclooxygenase 2 blocks human cytomegalovirus replication
- in intestinal myofibroblasts, IL-1-mediated induction of COX-2 expression is a complex process that requires input from multiple signaling pathways.
- COX-2 is an independent prognostic factor for poor survival (relative risk, 2.74; 95% CI, 1.38 to 5.47) in ovarian carcinoma.
- co-stimulatory mechanisms may exist that increase the expression of cox-2 and laminin-5 at the invasive front of lung adenocarcinomas and that EGFR signaling could be one of the mechanisms
- the effects of several paracrine and/or autocrine signaling pathways in the regulation of expression of aromatase, COX-1, and COX-2 in breast cells has identified complex relationships
- overexpresssion in HER-2 positive breast cancer with involvement of AP-1 and PEA3
- 4-(4-cycloalkyl/aryl-oxazol-5-yl)benzenesulfonamides as selective cyclooxygenase-2 inhibitors
- Overexpression of cyclooxygenase-2 (COX-2) in human primitive neuroectodermal tumors
- Reduced prostate cancer growth after exposure to saw palmetto extract may relate to decreased expression of Cox-2
- greater expression seen in adenocarcinoma rather than squamous cell carcinoma of lung; no correlation seen between increased expression and major clinicopathologic factors
- highly expressed in adenoma and adenocarcinoma in intraductal papillary-mucinous tumors of the pancreas
- overexpression of COX-2 and iNOS were revealed in epithelial cells of lymphocytic thyroiditis and thyroid tumors
- In advanced gallbladder carcinoma, enhanced expression of cyclooxygenase-2 is observed in the adjacent stroma.
- COX-2 is upregulated in endometrial cancer and facilitates tumor growth via angiogenesis produced in associated with VEGF and TP
- Cyclooxygenase-2, player or spectator in cyclooxygenase-2 inhibitor-induced apoptosis in prostate cancer cells
- Cyclooxygenase-2 (COX-2), epidermal growth factor receptor (EGFR), and Her-2/neu are expressed in ovarian cancer.
- COX-2 appears to be constitutively and selectively present in medullary epithelial cells of the human thymus.
- The MEK/ERK pathway mediates COX-2-selective NSAID-induced apoptosis and induced COX-2 protein expression in colorectal carcinoma cells
- Serous cystadenocarcinomas also had an unexpectedly high expression of COX-2.
- malignant endometrial epithelial cells secrete PGE(2) that induces COX-2 expression in normal endometrial stromal cells in a paracrine fashion through activation of transcription and stabilization of COX-2 mRNA
- induction of promoter activity by deoxycholic acid
- results suggest that NFkappaB is involved in the IL-1beta-induced COX-2 expression in the mesenchymal cells of human amnion
- expression is induced during human megekaryopoiesis and characterizes newly formed platelets
- expression induced by interleukin-1beta and amyloid beta 42 peptide is potentiated by hypoxia in primary human neural cells
- cyclooxygenase gene expression in human preimplantation embryos.
- data collectively imply COX-2 may play an important role during premalignant hyperproliferation, as well as the later stages of invasive carcinoma and metastasis in various human epithelial cancers
- Cholesterol-sensitive transcriptional pathways that regulate COX-2 expression are present in vascular tissue.
- Cox-2 could participate in the carcinogenic process of oral mucosa
- PI3K destabilizes cyclooxygenase 2 mRNA
- increased expression associated with development of lung cancer and possibly acquisition of invasive/metastatis phenotype
- Inhibitory effect of a selective cyclooxygenase-2 inhibitor on liver metastasis of colon cancer.
- COX-2 may be involved in inflammatory responses in chronic pancreatitis and in the progression of this chronic inflammatory disease.
- ERBB-2 overexpression and cyclooxygenase-2 up-regulation in human cholangiocarcinoma and risk conditions.
- PGHS-2 has a role in regulating PGE2 expression in human thyrocytes
- expression in pancreatic adenocarcinoma and pancreatic intraepithelial neoplasia
- These results support a functional role for peroxide-generated tyrosyl radicals in lipoxygenase catalysis by aspirin-treated prostaglandin h synthase-2 (ASA-PGHS-2).
- increassed expression in squamous cell carcinomas of the head and neck
- Data indicate that both COX-1 and COX-2 contribute to endothelial prostanoid synthesis in the neonatal human brain under basal conditions and in response to proinflammatory cytokine IL-1 beta.
- Both PAR1 and PAR2 upregulate COX-2, but not COX-1, expression in HUVEC cells
- tobacco smoking associated with COX-2 gene over-expression in human urinary bladder and concomitant increase in prostaglandin synthesis
- Protein kinase C-epsilon mediates bradykinin-induced cyclooxygenase-2 expression in human airway smooth muscle cells
- COX-2 is expressed in a high percentage of a large series of primary endometrial tumors and its expression may be associated closely with parameters of tumor aggressiveness
- COX-2 overexpression can be used as a potent molecular risk factor in patients with FIGO Stage IIB SCC of the uterine cervix who are treated with radiotherapy and concurrent chemotherapy.
- Human fallopian tubes express prostacyclin (PGI) synthase and cyclooxygenases and synthesize abundant PGI
- examination of a large series of human PJS polyps revealed that COX-2 was highly up-regulated in the majority of these polyps
- mediation by NF-kappa B and Ku70 or Ku80
- NFkappaB transcription factor is a key regulator of COX-2 expression in TNF-alpha-induced PGE2 production
- Cyclooxygenase-2 functional promoter variants may influence susceptibility to acute and chronic inflammatory diseases.
- The overexpression of COX-2 in well-differentiated HCC suggests that COX-2 may play a role in the early stages of hepatocarcinogensis.
- in human pulmonary epithelial cells, IL-1beta activates ERK or p38 to induce COX-2 production, which in turn induces MUC2 and MUC5AC production.
- Cyclooxygenase-2 acts as an endogenous brake on endothelin-1 release by human pulmonary artery smooth muscle cells: implications for pulmonary hypertension.
- HGF may stimulate the progression and growth of tumor cells in vivo by induction of Cox-2
- Autocrine/paracrine prostaglandin E2 production by non-small cell lung cancer cells regulates matrix metalloproteinase-2 and CD44 in enzyme-dependent invasion
- mediates the proliferative action of mast-cell tryptase: possible relevance to human fibrotic disorders
- PGE(2) production via a COX-2-catalyzed pathway plays a critical role in HIF-1alpha regulation by hypoxia; COX-2 inhibitors can prevent hypoxic induction of HIF-mediated gene transcription
- expression correlates with uPAR levels and is responsible for poor prognosis of colorectal cancer
- Induction of COX-2 may contribute to the inhibition of hypoxia-induced pulmonary vascular remodeling.
- COX-2 influences APP processing and promotes amyloidosis in the brain
- abnormal expressions of COX-2, p53, PCNA, and nm23 associate with malignant potential, lymph node metastasis and clinical stage, and they might therefore play a role in development of gastric cancer
- Data show that nitric oxide produced by inducible nitric oxide synthase (iNOS) increases the activity of cyclooxygenase-2 (COX-2) pathways in head and neck squamous cell carcinomas, and this effect is probably mediated by endocellular cGMP.
- inducible nitric oxide synthase-cyclooxygenase 2 interactions are involved in tumor cell angiogenesis and migration
- induction of astrocytic COX-2 is implicated in the pathogenesis of hippocampal sclerosis in temporal lobe epilepsy and is consistent with the previous findings of increased concentrations of prostaglandins in the cerebrospinal fluid of these patients
- role in protein kinase C beta II-mediated colon carcinogenesis
- induced in Ras-transformed human mammary epithelial cells undergoing apoptosis
- Helicobacter pylori strains show differences in activating transcription factors and induction of cyclooxygenase-2 (COX-2) gene in gastric epithelial AGS cells
- Results demonstrate the ability of hepatitis B virus X protein to promote tumor cell invasion by a mechanism involving the upregulation of membrane-type 1 matrix metalloproteinase (MT1-MMP) and cyclooxygenase-2 (COX-2).
- COX-2 gene expression is activated by protein tyrosine phosphatase inhibitors in human T lymphocytes
- The COX-2 expression in PC-3 High Invasive cells was approximately 3-fold higher than in PC-3 Low Invasive cells while the COX-1 expression was similar in both cell sublines.
- Thrombin upregulates COX-2-derived prostaglandin E2 synthesis by both catalytic cleavage of proteinase-activated receptor 1 and bFGF-dependent noncatalytic activity
- Results indicate that the cyclooxygenase-2 rather than the cyclooxygenase-1 gene is transcribed consistently in cultivated human iridial melanocytes of both blue and hazel eyes.
- a "defective" IL-1ra response to IL-1 may underlie, at least in part, the exaggerated prostaglandin-endoperoxide H synthase (PGHS)-2 induction in orbital fibroblasts
- Association of cyclooxygenase-2 expression with Hp-cagA infection in gastric cancer.
- Expression of cyclooxygenase-2 and clinicopathologic features in human gastric adenocarcinoma. Expression of COX-2 mRNA in gastric carcinoma was significantly higher. Staging classification was significantly correlated with COX-2 over-expression.
- The pathway of this enzyme is potentially involved in the regulation of tumor-associated angiogenesis and growth in pancreatic cancer
- upregulation of cytosolic phospholipase A2 and cox-2 in peripheral polymorphonuclear leukocytes during childhood bacterial infection increases thromboxane synthesis, which may contribute to acute inflammatory reaction
- Tristetraprolin binds to the 3'-untranslated region of cyclooxygenase-2 mRNA
- overexpression of cyclooxygenase-2 and vascular endothelial growth factor is associated with pancreaticobiliary maljunction
- Abnormal interleukin 10Ralpha expression contributes to the maintenance of elevated cyclooxygenase-2 in non-small cell lung cancer cells.
- Correlation of COX-2 and Ep-CAM overexpression in human invasive breast cancer and its impact on survival.
- COX-2 is induced by mucins in colonic neoplasms
- The abnormal expression of CEA and COX2 plays a role in the carcinogenesis and development of colorectal cancer.
- results collectively suggest that aberrant expression of microsomal prostaglandin E synthase-1 in combination with cyclooxygenase-2 can contribute to tumorigenesis
- Exposure to a cytotoxic concentration of gp120 up-regulates expression of the inducible isoform of cyclooxygenase (COX-2) in neuroblastoma cells and this is blocked by caspase 1 inhibitors
- Expressed in endocrine tumors of the pancreas.
- Cyclooxygenase-2 expression in small mesenteric arteries from patients with Crohn's disease.
- Salmonella infection rapidly increases Cox-2 expression in human intestinal tissue, accounting for increased epithelial ion transport characteristic of infectious diarrhea
- Activity is modulated in colorectal carcinoma cells.
- Knocking out this enzyme affects body temperature regulation.
- cyclooxygenase 1 and cyclooxygenase 2 enzyme immunoreactivity is present only in the neoplastic C-cells of medullary carcinoma
- COX-2 overexpression may play a crucial role in the carcinogenesis, development of cancer and lymph node metastasis in breast cancer patients.
- COX-2 may play a regulatory role in the proliferation of gallbladder epithelium, which may lead to carcinogenesis in patients with anomalous arrangement of the pancreaticobiliary duct.
- There is a correlation between expression of cyclooxygenase-2 and angiogenesis in human gastric adenocarcinoma.
- hypermethylation of the CpG island in the cox-2 gene is a major mechanism that mediates transcriptional silencing in a subset of gastric cancers
- Results suggest that expression of cyclooxygenase-2 is not correlated with clinicopathologic and biologic features of ampulla of Vater cancer.
- COX-2 upregulation contributes to oesophageal squamous carcinogenesis in head and neck cancer patients.
- activation may be one of the distinct host degradative pathways in the pathogenesis of microbial-induced pulpal/periapical inflammation
- COX-1 and COX-2 protein expression levels were determined in sets of tumor and normal colon tissue
- hypothesis of association between COX-2 overexpression and expression of IL-1beta, IL-6 and the NF-kappaB subunit p65 in human colorectal cancer
- biochemical pathway exists wherein fluid shear activates cyclooxygenase-2, via a c-Jun N-terminal kinase2/c-Jun-dependent pathway, which in turn elicits downstream prostaglandin EP2 and EP3a1 receptor mRNA synthesis
- COX-2 expression is significantly more common in endometrial adenocarcinoma and ovarian serous cystadenocarcinoma, but not in cervical squamous carcinoma, compared with normal tissue.
- Cyclooxygenase-2 expression is related to nuclear grade in breast ductal carcinoma in situ and is increased in its normal adjacent epithelium.
- biosynthesis induced by fluid shear stress
- airway smooth muscle cells from asthmatic patients produce significantly less PGE2 and COX-2 compared with nonasthmatic cells.
- Endogenous factors drive PGHS-2 gene transcription in the chorion, and the stable PGHS-2 mRNA accumulates in the tissue at term.
- regulation of expression by ATP
- Prostaglandin E(2) production via mechanotransduction in bone cells proceeds via activation of COX-2, but not COX-1.
- COX-2 is related to tumor angiogenesis in gastric cancer.
- Orthotopic implantation of a colon cancer xenograft induces high expression of cyclooxygenase-2.COX-2 plays an important role in organ-specific liver metastasis of colon cancer.
- unknown factors besides Abeta deposition are necessary for the cyclooxygenase-2 up-regulation and neurodegeneration in Alzheimer's disease
- IKKalpha and NF-kappa B involved in COX-2 induction in colorectal tumors; COX-2 expression is an early postinitiation event
- Cox-2 was established as a specific tumour marker for melanoma of potential interest for targeted therapeutics.
- Bile salts or acidic conditions, or both, can induce COX-2 expression in normal pharyngeal mucosa, which implies that laryngopharyngeal reflux has a role in the tumorigenesis of the upper aerodigestive tract.
- Elevated expression of cyclooxygenase-2 is a negative prognostic factor for disease free survival and overall survival in patients with breast carcinoma.
- In this study, we have used quantitative PCR to analyse expression of beta-tubulin III, stathmin, RRM1, COX-2 and GSTP1 in mRNA isolated from paraffin-embedded tumor biopsies of 75 nonsmall-cell lung cancer patients treated as part of a randomized trial
- Troglitazone, peroxisome proliferator-activated receptor gamma ligand, inhibits growth of HepG2 cells and induces apoptosis. COX-2 mRNA and protein and Bcl-2 was down-regulated. Bax and Bak was up-regulated. Activity of caspase-3 was elevated.
- Cyclooxygenase-2 may be associated with tumor progression by madulating the angiogenesis in colorectal cancer tissue.
- Inhibition of proliferation and induction of apoptosis in human cholangiocarcinoma cells by cyclooxygenase-2 specific inhibitor celecoxib may involve COX-dependent mechanisms and PGE2 pathway.
- cyclo-oxygenase-2 specific mechanisms are responsible for the exercise-induced increase in prostaglandin synthesis
- COX-2 has a role in generating prostaglandin e2 which increases VEGF secretion in human pancreatic cancer
- COX-2 is induced in retinal astrocytes in human diabetic retinopathy, in the murine and rat model of ischemic proliferative retinopathy in vivo, and in hypoxic astrocytes in vitro. COX-2 but not COX-1 inhibitors prevented intravitreal neovascularization
- Production of PGE2 was inhibited by a selective cyclooxygenase-2 inhibitor, celecoxib.
- mPGES-2 is a unique PGES that can be coupled with both COXs and may play a role in the production of the PGE2 involved in both tissue homeostasis and disease.
- Gene expression in monocytes is regulated by ligation of the AGE receptor.
- Differential activation of subtype purinergic receptors modulates Ca(2+) mobilization and COX-2 in human microglia.
- Il-1beta induces this enzyme's expression in colon cancer cells through signal transduction and NFKB.
- COX-2 protein and mRNA were not detected in U937 cells, and their levels remained undetected during the entire course of treatment with retinoic acid.
- COX-2 has a role in development of neovasculature of human breast adenocarcinomas
- role for NF-kappaB in the co-ordinate induction of COX-2, mPGES and in the corresponding release of PGE2 by IL-1beta
- potential involvement transplant rejection
- p38 MAPK and NF-kappaB signaling regulate steady-state levels of COX-2 expression, p38 MAPK additionally affects stability of COX-2 mRNA in cytokine-stimulated human airway myocytes
- Data describe the correlation between inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 activities and p53 gene status in head and neck squamous cell carcinomas in vivo and in vitro.
- VEGF is one of the principal factors produced by hypoxic myocytes that is responsible for the induction of endothelial cell COX-2 expression.
- p38 MAPK activation inhibited the deadenylation of reporter mRNAs containing either the cyclooxygenase-2 or tumor necrosis factor AU-rich elements
- COX-2 and VEGF are expressed in head and neck squamous cell carcinoma and may have a role in tumor invasiveness and angiogenesis
- COX-2 or VEGF, but not cyclin D1 may play roles in breast cancer with poor prognosis
- Data suggest that TIA-1 functions as a translational silencer of cyclooxygenase-2 (COX-2) expression and support the hypothesis that dysregulated RNA-binding of TIA-1 promotes COX-2 expression in neoplasia.
- increases in COX-2 expression and enzymatic activity, which can occur in aging and in pathological states can lead to downstream cellular changes that have a negative impact on neuronal survival in cerebrovascular disease
- human breast tumours aberrantly express significantly higher levels of COX2; lobular carcinomas had a higher level of COX2 than ductal carcinomas.
- Transcription of the COX-2 gene in endometrial stromal cells is regulated by malignant endometrial epithelial cells.
- association of a promoter variant in the inducible cyclooxygenase-2 gene (PTGS2) with type 2 diabetes mellitus in Pima Indians
- up-regulation of cyclooxygenase-2 is associated with transitional and squamous cell carcinoma of the bladder
- Mixed-cell tumours, representing majority of uveal melanomas, may be further subclassified according to COX-2 expression, a marker of poor prognosis. Role in uveal melanoma should be further elucidated. COX-2 inhibitors may be adjuvant treatment.
- Cox2 may be involved in an early stage of squamous carcinogenesis of the esophagus and expression is related to cell division and dysplasia.
- COX-2 exerts a negative feedback on the expression of cathepsin D to reduce the generation of the antiangiogenic factor angiostatin, hence promoting a proangiogenic environment.
- COX-2 may play an important role in the early stage of carcinogenesis, and its expression in colorectal cancer is not associated with clinicopathological features and patients' prognosis.
- results indicate that activation of eicosanoid synthesis by cyclooxygenase-2 expression in chondroblastomas is probably an important factor inducing peritumoral inflammatory changes in chondroblastomas
- Over expression of COX-2 in reflux nephropathy suggests that COX-2 may be involved in the pathogenesis of tubulointerstitial damage associated with severe reflux nephropathy.
- High COX-2 expression in extragenital endometriosis is believed to be strongly correlated with the pathological abnormalities of this disease.
- expression of COX-1 and COX-2 may influence Amyloid beta peptide generation through mechanisms that involve PG-E2-mediated potentiation of gamma-secretase activity
- COX-2 expression was dramatically increased in the spinal cord of patients with ALS.
- Hyperglycemia increases mitochondrial ROS production, resulting in NF-kappaB activation, COX-2 mRNA induction, COX-2 protein production, and PGE2 synthesis. Might contribute to pathogenesis of diabetic nephropathy.
- COX-2 induction by bradykinin in human pulmonary artery smooth muscle cells is mediated by the cyclic AMP response element through a novel autocrine loop involving endogenous prostaglandin E2, EP2 receptor, and EP4 receptor
- An important role of COX-2 in Helicobacter pylori pathogenesis is dysregulation of the immune response.
- RTPCR showed that the NS398 antitumor effect was associated with COX-2 transcription inhibition. Importantly COX-2 expression was enhanced by irradiation but this phenomenon was abolished when cells were exposed to NS398.
- Cyclooxygenase-2 upregulates vascular endothelial growth factor expression and angiogenesis in human gastric carcinoma
- COX-2 expression is down-regulated in cervical and vulvar tumor cells invading the regional lymph nodes with respect to primary tumors
- H. pylori LPS is of low biological activity when compared with E. coli LPS in its ability to induce the expression of cyclooxygenase 2 and synthesis of prostaglandin E2
- methylation of not the exon-1 region but of the promoter region is important to regulation of Cox-2 gene expression
- cell-cell contacts induce an actively programmed necrotic process that functionally involves COX-2, a known hallmark of inflammation and cancer
- cyclooxygenase-2 is upregulated by p38 MAPK in tumor cells
- NO can be associated with carcinogenesis through the upregulation of COX-2
- COX-2 in mesenchymal cells induced by H. pylori may play an important role in the tumorigenesis of human hyperplastic gastric polyps
- changing Leu-384 (into Phe, Trp), Trp-387 (Phe, Tyr), Phe-518 (Ile, Trp, Tyr), and Gly-526 (Ala, Ser, Thr, Val) impaired or abrogated PGG2 synthesis, and typically 11R-HETE was the main product formed
- sodium butyrate inhibits angiogenesis through down-regulation of COX-2 expression and prostaglandin (PG)E2 and PGI2 production
- Stabilization of survivin may contribute to the apoptosis resistance effect of COX-2 in non-small cell lung cancer.
- Cyclooxygenase 2 gene polymorphism is associated with non-small cell lung cancer.
- Overexpression of COX-2 plays crucial role in carcinogenesis and development of extra-hepatic cholangiocarcinoma, indicating that COX-2 may serve as target for chemoprevention of extra-hepatic cholangiocarcinoma.
- Expression of Cox-2 is elevated in gastric adenocarcinomas, which correlates with several clinicopathological parameters, including depth of invasion and lymph node metastasis.
- As NO regulates COX activity in various cells, we investigated the effect of NO-donors and the novel NO-aspirin NC-4016 on human monocyte COX-2.
- COX-2 has a role in up-regulating the synthesis of TFPI-2 along with thrombin and PAR-1 signaling
- differential catalytic regulation of the two PGHS isoforms
- p300 is the predominant coactivator that is essential for COX-2 transcriptional activation by proinflammatory mediators.
- cross-linking of the RelA subunit of NF-kappa B but not C/EBP beta to the cox-2 promoter and flanking sequences after IL-1 treatment
- increased COX-2 expression and activity, contributes to the pathogenesis of B cell lymphomas
- findings suggest that high level monocyte prostaglandin synthase 2 expression is present in at-risk subjects at an early age and is maintained during progression to and after type 1 diabetes onset
- Increase in Cox-2 expression is correlated with the loss of epithelial basement membrane in morphologically normal areas
- Pontin52/TIP49a promotes COX-2 expression in tissue culture and is overexpressed in colon cancer tissue, co-localizing with COX-2 expression in transformed tissue, relative to paired normal tissue
- Cyclooxygenase-2 overexpression may be a feature of the aggressive phenotype and may be useful as a prognostic indicator in breast cancer.
- COX-2-dependent prostanoids may play an important role in the regulation of hypoxia-induced Ang2 expression
- role in regulating angiogenic switch
- COX-2 may have a role in cellular proliferation in human renal cell carcinoma
- Overexpression of COX-2 plays an important role in tumor progression of gastric cancer and in the early development/promotion of gastric carcinoma and is associated with H pylori infection.
- Evaluation of COX-2, VEGF and the microvessel density may give additional prognostic information for first-line chemotherapy and clinical outcome of patients with ovarian carcinoma.
- COX-2-mediated cross-linking may inhibit Abeta catabolism and possibly generate toxic intracellular forms of oligomeric Abeta
- TXA2 produced by COX-2 plays an important role in megakaryocytopoiesis.
- Expression of cyclooxygenase (COX)-2 is related to poor prognosis in ovarian carcinoma.
- Cyclooxygenase type-2 expression is upregulated in in situ breast cancer and is associated with surrogate markers of an aggressive DCIS phenotype including nonoestrogen-regulated signalling pathways
- COX-2 up-regulates VEGF-C and promotes lymphangiogenesis in human lung adenocarcinoma via the EP(1)/Src/HER-2/Neu signaling pathway.
- increased cyclooxygenase-2 expression in the endometriotic ovarian cyst wall was observed
- Studies with the COX-2-selective inhibitor NS-398 confirmed the COX-2 dependency of the later increase in prostanoid production
- Glucose-induced induction of COX-2 in human islets suggest that this is one route through which hyperglycemia may contribute to beta-cell dysfunction
- variation of the COX-2 promoter may influence the risk and development of prostate cancer
- expression of COX-2 may be induced in serous ovarian carcinomas by loss of tumor suppressor genes such as p53 and SMAD4 and by amplification of HER-2/neuoncogene
- COX2 and some prostanoids play a key role in IL-1beta-induced angiogenesis
- COX-2 and mPGES-1 are overexpressed in squamous cell carcinoma of the penis
- costimulatory effect of DEP & LPS led to enhanced production of COX-2 protein and to increased release of prostaglandin E(2); the effect was specific
- EGFR and COX-2 cooperate to promote cervical neoplasm progression
- COX-2 expression was accompanied by DC synthesis of PGE2, in activated dendritic cells
- HER-2 oncogene expression is regulated by COX-2 and prostaglandin E2.
- High glucose treatment of THP-1 monocytic cells led to a significant three- to fivefold induction of COX-2 mRNA.
- effect of the human flavonoid plasma metabolites (quercetin 3'-sulfate, quercetin 3-glucuronide and 3'-methylquercetin 3-glucuronide) on expression of COX-2 mRNA in human lymphocytes ex vivo using TaqMan real-time RT-PCR
- Cyclooxygenase-2 may be involved in the early stage of squamous carcinogenesis of the esophagus, and may be a target of prevention and treatment for esophageal squamous cell carcinoma.
- Neuronal COX-2 expression in all CA1-4 in the hippocampus was significantly up-regulated in the ALSD group, and, to lesser degree but significantly, in the ALS group.
- COX-2 has a role in colorectal tumorigenesis [review]
- These data suggest that the 3'-untranslated of the cyclooxygenase-2 (COX-2) gene is involved in not only the induction by lipopolysaccharides but also the suppression by dexamethasone of COX-2 expression at the post-transcriptional level.
- Up-regulation of cyclooxygenase 2 correlates with vascular endothelial growth factor expression and tumor angiogenesis in HBV-associated hepatocellular carcinoma
- COX-2 mrna expression in peripheral blood monocytes showed marginal increase in eary postoperative period.
- COX-2 may be valuable both as a prognostic factor and as a therapeutic target in melanoma.
- haplotype analysis showed a genetic association between the PTGS2 gene and schizophrenia
- COX-2 overexpression coincides with focal areas of p16INK4a hypermethylation in vivo, creating ideal candidates as precursors to breast cancer
- COX-2 may play a role in the advanced stages as well as early stages of hepatocarcinogenesis
- We propose that a component of the cytokine-induced Cox-2 mRNA stabilization pathway is sensitive to acetylation.
- Cox-2 and TBXAS may play an important role in pituitary tumor development and progression
- Thirty-eight colon carcinomas were analyzed by immunohistochemistry for cell adhesion molecules (E-cadherin, beta-catenin, CD44), cell cycle regulatory proteins (cyclin D1, p27, p21), mismatch repair proteins (hMLH1, hMSH2), cyclooxygenase-2 and DPC4
- renovascular COX-2 expression was a constitutive feature encountered in human kidneys at all ages, whereas COX-2 was seen in macula densa only in fetal kidney.
- COX-2 activity is stimulated by nitric oxide in colorectal cancer
- Assessment of COX-2 status in both tumor and stroma compartment could provide valuable information to identify cervical cancer patients endowed with a very poor chance of response to neoadjuvant treatment and unfavorable prognosis.
- We found that the -765G-->C polymorphism of the COX-2 gene is associated with a decreased risk of MI and stroke.
- Basic calcium phosphate crystals may be an important amplifier of PGE(2) production through induction of the COX enzymes and the proinflammatory cytokine IL-1beta.
- COX-2 is upregulated in the majority of cases of squamous dysplasia and squamous cell carcinoma of esophagus.
- Expression in esophageal squamous cell carcinomas related to COX-2 expression. Also associated with depth of primary tumor, stage, and probably lymph node metastasis. May assist in management planning.
- COX-2 may have proinflammatory and antiinflammatory properties as a function of expression of downstream PGH2 isomerases.
- In hepatocellular carcinoma cells, cell growth was largely retarded by Cox-2 upregulation via promoter demethylation.
- cox-2 gene expression is manifest in laryngeal cancer
- Polymorphisms in cyclooxygenase 2 is associated with colorectal cancer
- the level of COX-2 mRNA was similar in all subjects with ripe and unripe cervix
- COX1, but not COX2, is induced during ATRA-dependent maturation and appears to contribute to myeloid differentiation both in vitro and ex vivo, and COX-1 activity may potentiate the differentiation of human acute promyelocytic leukemia
- NADPH oxidase has a role in Cox-2 inhibition through ROS and GSH/GSSG reduction, and NF-kappaB suppression
- EGCG-induced COX-2 expression is mediated by phospholipase D isoforms through PKC and p38 in immortalized astroglial line and normal astrocyte cells
- TGF-beta superfamily is part of an autocrine/paracrine system involved in the regulation of COX-2 expression in the distal pulmonary circulation
- Fibronectin stimulates human lung carcinoma cell proliferation and diminishes apoptosis by inducing COX-2 gene expression and PGE2 biosynthesis.
- iNOS and COX-2 may play a synergistic role in the pathogenesis of gastric MALT lymphoma.
- half of the cases expressed iNOS and COX-2, but these two enzymes do not seem to be the key step in angiogenesis or carcinogenesis of pancreatic adenocarcinomas.
- COX2 may be an important factor in promoting tumour progression in ER-negative tumours and a potential drug target in breast tumours.
- Acid-induced activation of both ERK and p38 causes a significant increase in COX-2 promoter activity, and acid-activated ERK stabilizes COX-2 mRNA in Barrett's esophagus
- normal human lung fibroblasts, when exposed to cigarette smoke constituents, elicit COX-2 expression with consequent prostaglandin synthesis
- COX-2 plays a key role in VEGF production in gastric fibroblasts stimulated by IL-1 in vitro, and angiogenesis induced by the COX-2-VEGF pathway might be involved in gastric ulcer healing.
- Our objectives were to determine the relationship between cyclooxygenase-2 and haematogenous spread to bone marrow in patients with colorectal carcinoma.
- COX-2 is overexpressed in ependymomas
- COX-2 may be an important factor for esophageal cancer and inhibition of COX-2 may be helpful for prevention and possibly treatment of this cancer.
- COX-2 expression was observed in 30 of the 68 tumor samples (44%).
- COX-2 expression might be an early event in gastric tumorigenesis and provide a advantage for tumor cell proliferation because of its vascular-rich microenvironment and escape from tumor cell apoptosis, especially in intestinal-type gastric carcinomas.
- COX-2 expression was not up-regulated in any subdivision of the hippocampus in the schizophrenia group
- COX-2 may be involved in the course of tumor angiogenesis of colorectal cancer and acts through VEGF.
- Expression of COX-2 mRNA was observed in muscle tissues from patients with idiopathic inflammatory myopathies suggesting a role in pathogenesis of this disease.
- cyclooxygenase-2 expression is stimulated by endoplasmic reticulum stress through activation of NF-kappaB and pp38 mitogen-activated protein kinase
- Overexpression of HuR in tumor tissue may be part of a regulatory pathway that controls the mRNA in breast cancer
- Cox-2 expression is highly variable in Dukes' C colorectal tumors.
- Findings lend support to the hypothesis that COX-2 overexpression represents an adverse prognostic event in human breast cancer
- cPLA2 has an influence on IL-8 and COX 2 gene and protein expression at least in part through PPAR-gamma
- COX-2 expression induced by H pylori infection is a relatively early event during carcinogenesis in the stomach.
- Increased expression of cyclooxygenase-2 is associated with colorectal adenomas
- COX-2 is a hitherto unknown target by which a cannabinoid induces apoptotic death of glioma cells.
- Overexpression of COX-2 in NSCLC cells enhanced the antiapoptotic and mitogenic effects of IGF-I and IGF-II, the autophosphorylation of the type 1 IGF receptor, increased phosphatidylinositol 3'-kinase activity, and decreased expression of IGFBP-3.
- vascular endothelial growth factor and thymidine phosphorylase expression was also associated with a significantly higher level of COX-2, as well as greater intratumoral microvessel density
- Review of COX-2 expression in squamous cell head and neck neoplasms.
- Review of COX-2 in lung cancer treatment. COX-2 plays a role in lung cancer and may be a marker of prognosis.
- phosphodiesterase 4 inhibitors regulate NFAT-dependent cyclooxygenase-2 expression in human T lymphocytes
- In situ processing of COX-2-overexpressing glioma by tumor-infiltrating dendritic cells induces a tolerogenic T cell response by means of generating a CD4+ T regulatory type 1 (Tr1) response.
- The correlation between COX-2 and invasive depth, MVD and invasive depth, COX-2 and MVD were analyzed. COX-2 expression was significantly related to the invasive depth of tumors.
- H. pylori induces COX-2 expression via activations of NF-kappaB, NF-interleukin 6, the cAMP response element.
- Catalytic NO consumption by PGHS-2 represents a novel interaction between NO and PGHS-2 that may impact on the biological effects of NO in vascular signalling and inflammation
- cyclooxygenase-2 has a role in cytokine-induced beta-cell dysfunction and damage
- R(+)-methanandamide induces COX-2 expression in human neuroglioma cells via a pathway linked to lipid raft microdomains
- Gene expression regulation plays a role in prognosis of ovarian carcinoma.
- Immunohistochemical results are compared with patient survival in order to verify COX-2 prognostic significance in 32 primary oligodendrogliomas.
- endothelial cell confluence regulates cyclooxygenase-2 and prostaglandin E2 production that modulate motility
- expression in urethral epithelium upregulated by Neisseria gonorrhoeae PorB IB and upregulation dependent on NF-kappaB activation
- COX-2 protein was induced at later stages of erythroblast development through a p38/MAPK-dependent pathway
- integrin-mediated cell adhesion and soluble integrin ligands contribute to maintaining COX-2 steady-state levels in endothelial cells
- Elevated Cox-2 expression in stromal cells in eutopic endometrium from patients with deep endometriosis may play a role in severe, endometriosis-related dysmenorrhea.
- COX-2-positive prostate cancer cells can have impaired p53 function even in the presence of wild-type p53 and that p53 activity can be restored in these cells via inhibition of COX-2 activity.
- COX-2 is a potential therapeutic target because COX-2 is expressed in renal cell carcinoma and associated cell populations such as endothelia and monocytes/macrophages.
- COX-2 contributes to CYP2C9-induced angiogenesis.
- ACE signaling may underlie the increase in COX-2 and prostacyclin levels in patients treated with ACE inhibitors.
- inducing expression of COX-2, colon cancers further target the prostaglandin biogenesis pathway by ubiquitously abrogating expression of 15-hydroxyprostaglandin dehydrogenase (15-PGDH)
- The expression of functionally active thrombomodulin in human smooth muscle cells depends on prostaglandins endogenously formed via the COX-2 pathway. This provides a new platelet-independent mechanism for the prothrombotic effects of COX-2 inhibitors.
- All ESCC (Esophageal Squamous Cell Carcinoma) displayed COX-2 overexpression. The use of COX-2 inhibitors might be a therapeutic alternative in ESCC.
- COX-2 appear to be yet another novel mechanism by which p53 could abate its own growth-inhibitory and apoptotic effects in humn tumors.
- cyclooxygenase-2 has a role in immunomodulation of endometrial carcinoma
- Expression of the gene in members of a large pedigree with familial polyposis syndrome.
- Edible plant extracts are likely to inhibit TPA-induced COX-2 expression through suppression of DNA binding of NF-kappaB.
- Expression of NFAT wild type protein or the active catalytic subunit of calcineurin transactivates COX-2 promoter activity, whereas a dominant negative mutant of NFAT inhibited COX-2 induction in colon carcinoma cell lines.
- COX-2 contributes to the expression of Skp2 and poor survival in human gastric carcinomas
- differentiation-inducing agents, particularly sodium butyrate, suppress growth of oral squamous carcinoma cells through apoptosis and induce cell differentiation possibly through mechanisms involving COX-2, p27Kip1 and/or p21WAF1/Cip1 in vitro and in viv
- high glucose, via PI3K/Akt signaling, induces NF-kappaB-related upregulation of COX-2, which in turn triggers the caspase-3 activity that facilitates vascular endothelium apoptosis
- gene expression regulation in Lyme disease
- Extracellular catalase induces COX2 in primary chondrocytes.
- Noncoplanar PCBs alter HL-60 cell function and COX-2 expression via an Ah-receptor-independent mechanism.
- Renal medullary oxygenation is improved by water diuresis in normal young women in a way that is blocked by a selective inhibitor of COX-2 as well as non-selective cyclooxygenase inhibitors.
- important role in the early stage of colorectal carcinogenesis
- COX-2 expression in both cancer cells and stromal cells within the lung cancer microenvironment may play an important role in upregulating the expression of the angiogenic factor VEGF in lung cancer.
- Taken together, these results suggest a novel function of COX-2 that inhibits DNA damage-induced apoptosis through direct regulation of p53 function.
- histone deacetylases regulate a transcriptional block on the Cox-2 and c-myc genes
- Results showed a stepwise increase in the expression of COX-2 as mucosal damage progressed from normal to gastritis to gastric ulcer.
- Cyclooxygenase-2 may have a role in progression of multiple myeloma
- High cyclooxygenase-2 expression is associated with breast cancer
- COX-2 may regulate expression of apoptosis suppressor gene (bcl-2) through interaction of tumor cells and stromal cells
- COX-2 has a role in response of esophageal squamous cell carcinoma to chemoradiotherapy
- The main signaling pathway for toxin A induction of human COX-2 involves ROS-mediated activation of p38 MAPK, MSK-1, CREB, and ATF-1
- the COX-2 T8473C polymorphism may contribute to lung cancer susceptibility in the Chinese population
- COX-2 is induced by RSV infection of human lung alveolar epithelial cells with the concomitant production of PGs
- Exposure of human uterine myocytes to both stretch and IL-1beta activates the MAPK system, which is responsible for the increase in PGHS-2 mRNA expression.
- PGH synthase-2, CYP4F8, and PGE synthase-1 likely forms 19-hydroxy-PGE compounds in seminal vesicles and vas deferens
- results suggest E1A-F is overexpressed in early stages of human CRC development and may be an important factor in the overexpression of COX-2 and MMP-7
- Atorvastatin down-regulates LPS-induced expression of the COX-2 and consequently inhibits production of PGE2 in cultured A549 cells.
- COX-2 overexpression in human breast cancer cells enhances cell motility and invasiveness thus suggesting a mechanism of COX-2 mediated metastasis
- The inhibition of the Cox-2 protein expression could serve as a means of muting the cellular inflammatory response during HCV infection.
- under specific conditions of cellular stress, a common variation in cyclooxygenase-2 promoter structure may enhance cyclooxygenase-2 transcription, and this may contribute to the proliferation of an inflammatory response in brain cells
- cyclooxygenase-2 enzyme expression differs in radiosensitive versus radioresistant glioblastoma multiforme cell lines
- Cyclooxygenase-2 (COX-2) is frequently expressed in papillary thyroid carcinoma but not in benign thyroid specimens
- Regulation of COX-2 may alter peritoneal healing and may provide the opportunity to reduce postoperative adhesion development.
- role in interleukin-1beta regulation of beta2 adrenoreceptor and prostaglandin E2-mediated cAMP accumulation and chloride efflux from Calu-3 bronchial epithelial cells
- Endothelin-1 stimulates cyclooxygenase-2 expression in ovarian cancer cells through multiple signaling pathways: evidence for involvement of transactivation of the epidermal growth factor receptor.
- induction of COX-2-expression is an important response of HUVEC to stimulation with rhAPC and may represent a new molecular mechanism, by which rhAPC promotes upregulation of prostanoid production in human endothelium
- Pharmacological and endogenous PPARG ligands use both receptor-dependent and -independent mechanisms to influence COX2 expression.
- epidermal growth factor receptor is activated by imatinib mesylate, resulting in cyclooxygenase-2 induction and prostaglandin E2 accumulation
- COX-2 is not a prognostic marker in squamous cell carcinoma of the esophagus, but low COX-2 expression is associated with poor prognosis in the neoadjuvant-treated patients.
- COX-2 overexpression in human breast epithelial cells will predispose the mammary gland to carcinogenesis.
- AHR pathway plays important role in cigarette smoke-mediated COX-2 and prostaglandin production in human lung fibroblasts and may contribute to tobacco-associated inflammation and lung disease.
- Data supports the cyclooxygenase-2/prostaglandin E2/hypoxia-inducible factor-1alpha/vascular endothelial growth factor pathway possibly contributing to tumor angiogenesis in gastric carcinoma.
- Findings suggest that COX-2 may be an effective therapeutic target in prostate cancer treatment.
- The generation and antifungal activity of hydroxyeicosanoids from 3-HETE by COX-2 are reported.
- Increased cyclooxygenase 2 expression is associated with papillary thyroid cancer
- Significantly higher expression of cyclooxygenase 2 is associated with metastasis in non-small cell lung cancer
- Alternative polyadenylation of COX-2 may be an important post-transcriptional regulatory event.
- Mitochondrial COX-2 in cancer cells confer resistance to apoptosis by reducing the proapoptotic arachidonic acid.
- The increased COX-2 expression in distal BE was not associated with inflammation in Barrett esophagus; COX-2 protein expression in the oesophagus appears to be independent of the degree of inflammation.
- Chemopreventive treatments were effective in inhibiting tumor development in NMBA-treated animals only when they reduced PGE2 levels in preneoplastic esophageal tissues approximately to those levels found in normal esophagus, by inhibiting Cox-2.
- role of COX-2 in regulating the degree of apoptosis by modulating bcl-2 protein in benign and malignant parotid gland tumors
- These results suggested that the combination of 5-FU and genistein exert a novel chemotherapeutic effect in colon cancers, and AMPK may be a regulatory molecule of COX-2 expression, further implying its involvement in cytotoxicity caused by genistein.
- cyclooxygenase-2/PGE2 may exert pro-oncogenic actions through stimulating the beta-catenin/T cell factor-mediated transcription, which plays critical roles in colorectal carcinogenesis
- data indicate that hepatitis C virus core suppresses IKK signalsome activity, which blunts COX-2 expression in macrophages
- Elevated expression of cyclooxygenase-2 in colorectal adenocarcinoma is associated with p53 accumulation and hdm2 overexpression
- Helicobacter pylori infection transactivates COX-2 promoter activity and increases the binding of NF-kappaB to this promoter.
- The demethylation of 5' CpG island of gene is necessary for COX-2 expression in human gastric cancer.
- COX-2 expression is an independent clinicopathologic factor and an independent prognostic factor in endometrial carcinoma.
- IL-1beta-induced cPLA2 and COX-2 gene expression is modulated through the p38 MAPK pathway in both neuroglioma and neuroblastoma cells.
- Altogether our findings revealed that IL-20 is a negative modulator of COX-2/PGE(2) and inhibits angiogenesis.
- novel anti-inflammatory property of recombinant HBsAg which involves inhibition of COX-2.
- Augmented tumor neovascularization induced by VEGF may be one of the several effects of COX-2 responsible for poor prognosis of human gallbladder carcinoma
- COX-2 upregulation showed to be a late event and in a multivariate analysis it was associated independently with a reduced survival after surgery compared with low COX-2 expressed esophageal tumors
- COX-2 may have a role in preventing relapse of endometriosis after laparoscopic ablation
- Histone deacetylase inhibitors suppress the induction of c-Jun and its target genes including COX-2
- Taken together, IFN-alpha-induced activations of NF-kappaB and COX-2 were inhibited by the addition of curcumin in A549 cells.
- Expression of COX2 is common in advanced urinary bladder cancer (BC) with poor prognostic characteristics, supporting efforts to initiate clinical trials on the efficacy of COX2 inhibitors in the adjuvant treatment of high-risk urinary BC.
- Inhibition of cyclooxygenase-2 suppresses invasiveness of oral squamous cell carcinoma cell lines via down-regulation of matrix metalloproteinase-2 and CD44
- The loss of TNF-alpha-regulated COX-2 expression in ovarian neoplasms is associated closely with epithelial neoplastic morphological transformation.
- T-oligos transcriptionally down-regulate COX-2 expression in human skin via activation and up-regulation of p53, at least in part by inhibiting NFkappaB transcriptional activation
- Vitamin E inhibited cyclooxygenase (COX) activity but did not affect the expression of Cox-2.
- MMP-1 expression by latanoprost requires prior up-regulation of COX-2
- COX-2 may play an important role in the regulation of pancreatic stellate cells proliferation in response to pancreatic cancer
- Genetic variants in COX-2 may play a role in mediating susceptibility to esophageal neoplasms.
- The increased prostacyclin biosynthesis in smokers is derived largely from the inducible COX-2.
- COX-2 may play an important role in the development of gastric cancer, and the over-expression of COX-2 protein may be a high risk factor for liver metastasis.
- Increased COX-2 expression is involved in gastric carcinogenesis, and may be necessary for maintenance of the malignant phenotype and contribute to Helicobacter pylori-associated malignant transformation.
- Data demonstrates that IL-1alpha and COX-2 mRNA are frequently co-expressed in human gastric cancer tissues, and suggest that the IL-1alpha-COX-2 pathway might be involved in tumor progression by regulating cancer cell proliferation.
- there is higher stromal COX-2 mRNA expression compared to that within the epithelium for colorectal adenomas and carcinomas
- cyclooxygenase-2 elevation is related to lymph node metastasis in adenocarcinoma of uterine cervix
- Under hypertonic but not under isotonic conditions, splice variant-specific degradation of Cox-1ir mRNA using RNA interference resulted in increased production of fully spliced Cox-2 mRNA.
- In this review, cyclooxygenase-2 is recognized as an important adverse prognostic factor that promotes multiple events involved in tumorigenesis.
- Expression in kidney is a useful maker for tumorigenesis of the renal call carcinoma in vivo.
- COX-2 expression was not correlated with clinicopathological characteristics of colon carcinoma and disease outcome.
- Ufavourable prognostic significance of COX-2 and MDR1/P-gp in breast cancer.
- COX-2 may be involved in carcinogenesis of the breast and may be an independent prognostic indicator in patients with invasive ductal carcinoma.
- Shear-induced cyclooxygenase (COX)-2 suppresses phosphatidylinositol 3-kinase (PI3-K) activity, which represses antioxidant response element (ARE)/NF-E2 related factor 2 (Nrf2)-mediated transcriptional response in human chondrocytes.
- Incidence of K-ras mutation and frequencies of COX-2 and gastrin overexpressand protruded type ion are high in laterally spreading granular colorectal tumors.
- CD40 ligand might contribute to the initiation and progression of atherosclerosis by increasing activity of prostacyclin synthase.
- Induction of COX-2 transcription induced by proteasome inhibitors requires reactive oxygen species-dependent protein kinases activation.
- histamine exerts both a proproliferative and a proangiogenic effect via H2/H4 receptor activation, mediated by increasing COX-2-related PGE2 production in COX-2-expressing colon cancer cells
- The COX-2-related pathway, which is essential in mediating cellular inflammatory response, is the critical signaling link for the bystander phenomenon.
- Patients with carotid atherosclerosis depict an overexpression of COX-2, mPGES-1 and EPs in blood mononuclear cells and plaque of patients with carotid atherosclerosis regulated by nuclear factor-kappaB
- Stromal myofibroblasts expressed COX-2 only in colon adenocarcinomas (100% of the cases) and not in normal colon.
- LPA acts upstream of various receptor tyrosine kinases and COX-2, and thus may act as a potent stimulator of colorectal cancer.
- High COX-2 is an independent prognostic factor in gastric cancer.
- Collectively, our results demonstrate that PGE(2) at physiologically relevant concentrations induces COX-2 expression in human NPE cells via activation of EP(2)- and EP(4) receptors and phosphorylation of p38 and p42/44 MAPKs.
- Allele 5209G was weakly associated with Crohn's disease (odds ratio (OR) 1.63, 95% confidence interval (CI) 1.03-2.57), and allele 8473T with ulcerative colitis (OR 1.50, 95%CI 1.00-2.27).
- Cyclooxygenase-2-dependent activation of STAT3 by interleukin-6 has a role in non-small cell lung cancer
- Oxalate exposure upregulates cyclooxygenase-2
- COX-2 overexpression likely represents an additional mechanism of resistance to apoptosis in B chronic lymphoid leukemia.
- functional and physiological significance of COX-2 in the placenta and in fetal development.
- These findings contribute to determine the key signalling pathways involved in the regulation of COX-2 expression in colorectal cells by inflammatory stimuli, such as IL-1beta.
- Findings disclose a cross-talk between the COX-2/PGE(2)/EP(1) and EGFR/c-Met signaling pathways that coordinately regulate human hepatocellular carcinoma cell invasion.
- hypoxia-elevated Ang-2 expression in gastric cancer cells may be mediated by both Cox-2-derived PGE2 and HIF-1alpha pathways
- Diabetic conditions such as advanced glycosylation endproducts and high glucose in vitro can upregulate the expression of the inflammatory PTGS2 gene in pancreatic islets.
- PPARalpha activators LY-171883 and WY-14,643 were able to diminish transcriptional induction of COX-2 and VEGF by inhibiting AP-1 (activator protein-1)-mediated transcriptional activation.
- COX-2 may be involved in an early stage of squamous cell carcinogenesis of the esophagus
- These results suggest that HRG might be a new member of the growth factor family involved in the COX-2-dependent ulcer repair process.
- a common PTGS2 variant increases bile duct cancer risk
- inhibition of GSK-3beta stimulates COX-2 expression in gastric cancer cells
- heparanase may play a novel role for COX-2 mediated tumor angiogenesis in breast-cancer progression
- EP1 receptor level increase in sensory neurones, and macrophage infiltration, appears to precede increased Cox-2 expression by macrophages in nerve injuries
- CCAAT/enhancer-binding protein beta (C/EBPbeta) DNA-binding sites are crucial for the function of the COX-2 gene promoter.
- p38 MAPK- and NF-kappaB-controlled COX-2 expression and subsequent PGE(2) release by lung epithelial cells may contribute significantly to the host response in pneumococcal pneumonia.
- Nm23-H1 and EBNA3C can modulate expression of COX-2 in the context of EBV infection and transformation.
- Data show that cyclooxygenase-2 mRNA and protein overexpression in hepatoma cell lines correlate with increased cell growth rate, which can be inhibited by celecoxib.
- EIncreased expression of cyclooxygenase-2 is associated with cutaneous melanoma progression
- inducible nitric oxide synthase and Cox-2 play an important role in the apoptosis induction in trophoblasts of human fetal membrane tissues
- COX-2 over-expression rate was greater in ovarian carcinoma that was associated with endometriosis than in isolated ovarian carcinoma.
- C allele of -765G>C COX-2 polymorphism was associated with lower COX-2 expression, and reduced subclinical atherosclerosis
- Expression of cyclooxygenase-2 enhances survival of chronic lymphocytic leukemia B cells.
- COX-2 showed a statistically significant difference between early-onset gastric cancers and conventional gastric cancers.
- in human colorectal carcinoma, vascular endothelial growth factor-C and cyclooxygenase-2 are coexpressed and significantly associated with lymph node metastasis and prognosis
- These results demonstrate that the inducible NFAT3-mediated iNOS upregulation represents a novel potent tumor-suppressing pathway and may contribute to the tumor suppressor functions of NFAT protein.
- The co-localization of COX-2 with Cav-3 in the caveolae suggests that the caveolins might play an important role for regulating the function of COX-2.
- Logistic regression analysis showed p53 and COX-2 as dependent predictors in pancreatic carcinogenesis, and a reciprocal relationship to neoplastic progression between p53 and COX-2.
- Data obtained demonstrate that the combination of arsenite with inhibitors of COX-2 may affect the target cancer cells via induction of FasL-mediated death signaling.
- Homozygous PTGS2 8473-CC genotype may be associated with breast cancer risk.
- data presented here provide evidence for the control of microsomal PGES-2 expression by cyclopentenone prostaglandins independently of upstream COX enzymes
- a selective induction of cox-2 in multiple myeloma cells containing RAS mutations, results in heightened binding to extracellular matrix protein and chemotherapeutic drug resistance
- Review. The genetic control of COX-2 expression and its implications for aromatase expression in normal and malignant breast tissue are examined.
- NFAT promotes breast cancer cell invasion through the induction of COX-2 and the synthesis of prostaglandins
- Study supports the hypothesis that inflammation is involved in prostate carcinogenesis and that sequence variation within the COX-2 gene influence the risk of prostate cancer.
- COX-2 may play a roll in tumor progression of epithelial ovarian cancers and contribute to tumor angiogenesis by stimulating VEGF expression
- COX-2 and EGFR may be cooperative in the stepwise progression from Barrett's esophagus to adenocarcinoma, thereby leading to carcinogenesis.
- Stress-induced upregulation of COX-2 gene expression in ARPE-19 and HN cells may play a mechanistic role in promoting proinflammatory and/or pro-oxidative pathology in these tissues.
- the COX-2 8473T>C polymorphism may have a role in development of adenocarcinoma of the lung
- Expression of both bcl-2 and cox-2 were increased in non-dysplastic Barr
- Up to half of MMR-deficient colorectal cancer do not show COX-2 overexprssion, and COX2 hypermethylation seems to be responsible for gene silencing in one third of them.
- role of COX-2 in carcinogenesis of gastrointestinal tract, such as the esophagus, stomach and colorectum [review]
- IL-4 has the capacity to inhibit COX-2 mRNA transcription in NSCLC cells and the inhibition of PGE(2) appears to be predominately COX-2 dependent.
- seminal plasma and PGE(2) can promote the expression of tumorigenic and angiogenic factors, in cervical adenocarcinoma cells via the EP4 receptor, EGFR, and ERK1/2 signaling pathways
- COX-2 up-regulation was significantly associated with sentinel lymph node and bone marrow micro-metastasis in breast cancer patients
- These findings demonstrate a coordinated induction of COX-2 and mPGES-1 by PDB/TG that proceeds through PKC/ERK and Ca2+ signaling cascades, resulting in increased PGE2 production.
- presence of irregular bleeding during oral contraceptive use is associated with strong cyclooxygenase-2 (COX-2) expression in the endometrium
- These results imply that native PGHS-2 exhibits half-of-sites reactivity.
- Data show that substance P stimulates production of prostaglandin E2 and receptor activator of nuclear factor- B ligand, and promotes bone resorption.
- COX-2 and 15-PGDH are regulated reciprocally in A549 cells
- Vaginal administration of the nitric oxide donor isosorbide mononitrate (IMN) induces increased cervical expression of COX-2;this pathway may act in cervical ripening at term.
- Increased cyclooxygenase-2 expression is correlated with suppressed antitumor immunity in cervical adenocarcinomas
- By affecting the expression rather than the activity of COX-2, these in vitro data reported herein give further evidence on the anti-inflammatory protection by procyanidins.
- p53 and NF-kappaB cooperate in upregulating Cox-2 expression, promoting cell survival in inflammatory precursor lesions.
- certain bile acids like chenodeoxycholic acid (CDCA) directly inhibit cell proliferation through an increased COX-2 expression and PGE2 synthesis
- Mutations in the APC gene resultt in impaired retinoic acid biosynthesis and upegulation of cox2.
- Forced COX-2 expression in gastric cancer cells did not inhibit apoptosis caused by NAG-1 expression.
- Gene expression data suggest that pharmacologic inhibition of COX-2 and VEGF may be useful adjuncts in targeted therapy for esophageal adenocarcinoma.
- These results indicate that the inhibition of cyclooxygenase-2 can lead to the regression of disseminated skin melanoma metastases, even after failure of chemotherapy.
- changes in COX-2 and Ki-67 expression peaked during the proliferative phase and fell during the late luteal phase in endometrial polyps and disease-free endometria
- our findings provide evidence of COX-2-independent targets promoting cell growth arrest and differentiation in cells lacking COX-2 expression at the mRNA level.
- The significant differences in COX-2 expression among normal epithelium, low-grade dysplasia and high-grade dysplasia suggest that overexpression of COX-2 enzyme is an early event in gallbladder carcinogenensis.
- COX-2 may play a key role in the development and progression of gastric adenoma
- study demonstrates that when cytomegalovirus replicates in retinal pigment epithelial cells, COX-2 induction augments virus replication via the PGE pathway
- This effect is statistically significant in lung cancer stage I, suggesting that COX-2 expression could be useful at early stages to distinguish those with a worse prognosis.
- Human prorenin receptor directly or indirectly contributes to the regulation of renal cortical COX-2 expression.
- Cyclooxygenase-2 is expressed in hamster and human pancreatic neoplasia
- COX-2 and p53 may have roles in microsatellite instability in colorectal cancer
- TGF-beta1 regulates COX-2 expression in human mesangial cells through the activation of ERK1/2, p38 MAPK, and PI3K.
- COX-2 expression is significantly increased in the ureteral wall in response to obstruction in the rat and human ureter and COX-2 activity contributes to increased pelvic pressure after obstruction.
- COX-2 is downregulated by PC-SPES via inhibition of NF-kappaB and C/EBPbeta in non-small cell lung cancer cells
- Cytoplasmic expression as well as nuclear translocation of PTGS2 increased with progression of oral cancer
- Thymomas and thymic carcinomas had a significantly stronger COX-2 expression than that of the normal thymus.
- there is a difference in the influence of COX-2 on response depending on treatment regimen
- Prostaglandin-endoperoxide synthase 2 (PTGS2) is a key regulatory enzyme in the synthesis of the antifibrotic agent prostaglandin E(2) and is reduced in sarcoidosis lung. A promoter polymorphism in PTGS2, -765G>C, is reported to reduce its expression.
- These results implicate COX-2 in the angiogenesis and biological aggressiveness of diffuse astrocytomas.
- Elevated non-esterified fatty acid (NEFA) induced COX-2 gene expression in cultured monocyte-derived macrophages.
- Study suggests that COX-2 enzyme is important regulator of bone mineral density and bone strength.
- prostaglandin-endoperoxide synthase 2 polymorphisms, prostaglandin-E receptor 2 polymorphisms, and C-reactive protein concentrations may have a role in atherothrombosis
- Overexpression of cyclooxygenase-2 correlates with tumor angiogenesis in endometrial carcinoma
- This hypothesis indicates a possible novel function of heparanase and its link to HIF1alpha and Cox-2, and therefore this function would give us a clue about potential new strategies for cancer therapy.
- Potent antitumor role of S100A2 in squamous cell carcinoma partly via reduced expression of COX-2.
- Reintroduction of wild-type LKB1 into cells induced down-regulation of PEA3 resulted in reduced cyclooxygenase-2 RNA and protein expression.
- Discoidin domain receptor family member 1-mediated Cox-2 induction is NF-kappaB dependent in breast cancer.
- In diabetic coronary arterioles bradykinin induces enhanced COX-2-derived prostaglandin-mediated dilation. May serve to increase dilator capacity and maintain adequate perfusion of cardiac tissues.
- Decreased PGI2S protein and mRNA in the lungs from patients with emphysema.
- R. rickettsii infection of human endothelial cells causes robust induction of COX-2 mRNA and protein expression.
- results suggest that COX-1 and COX-2 activities are decreased in the placental tissue of women with pre-eclampsia, probably by oxidative stress
- Lipopolysaccharide-induced up-regulation of COX-2 depends on the activity of the Mg(+2)-dependent phosphatidic acid phosphohydrolase 1 (PAP-1)
- Intestinal epithelial cell lines up-regulated Cox-2 expression in a TLR4- and MyD88-dependent fashion.
- Results show that alpha2beta1 integrin signalling enhances cyclooxygenase-2 expression in intestinal epithelial cells.
- The results demonstrated statistically significant increased oral mucosal staining for NF-kappaB and COX-2 following cytotoxic chemotherapy and provide further support for the role of NF-kappaB and COX-2 in the pathogenesis of mucositis.
- This study failed to demonstrate any prognostic significance of COX-2 expression alone or co-expression with HIF-1alpha or VEGF in advanced NPC.
- COX-2 induction by nickel compounds occurs via an IKKbeta/p65 NF-kappaB-dependent but IKKalpha- and p50-independent pathway and plays a crucial role in antagonizing nickel-induced cell apoptosis in Beas-2B cells
- These studies suggest that SZ95 sebocytes express functional PAF-Rs and PAF-Rs are involved in regulating the expression of inflammatory mediators, including COX-2, PGE(2) and IL-8.
- Data demonstrate that cyclooxygenase-2 directly regulates gene expression of specific aromatase promoter regions and regulates aromatase enzyme activity.
- Findings demonstrate that activated platelets induce COX-2 synthesis in monocytes by combinatorial signaling to transcriptional and posttranscriptional checkpoints.
- a cyclooxygenase-2 amino acid cassette mediates entry of the protein into the endoplasmic reticulum-associated degradation system
- Activated T cells highly express Cox-2 and synthesize prostaglandin D2 and related prostaglandins that are PPAR-gamma ligands.
- The -765G > C COX-2 polymorphism should be considered as another susceptibility marker for gastric adenocarcinoma development in patients with atrophy or intestinal metaplasia.
- Human labor is associated with increased expression of COX-2 in the myometrium.
- Transfected COX-2 gene delivery protects neurons from DNA damage induced by oxidative, genotoxic, and excitotoxic stresses and by ischemic injury.
- PKCalpha and p38 and p42/44 MAP kinase controlled COX-2 expression and subsequent PGE(2) release by Legionella-infected lung epithelial cells. These pathways may significantly contribute to the host response in Legionnaires' disease.
- Cyclooxygenase-2 has a role in progression of metastatic melanoma
- Overexpression of COX-2 elevated tumorigenicity, tumor growth and invasion of human KB carcinoma cells via up-regulated MMP and Rho family small GTPases and down-regulated TIMP activities.
- Aldose reductase is an obligatory mediator of growth factor-induced up-regulation of COX-2.
- The endothelial cell response to hypoxia involves increased production of the anti-thrombotic eicosanoid, PGI(2), which is dependent on COX-2 upregulation by a HIF-mediated process.
- Results suggest that irrespective of the underlying disease, lung injury that causes extensive fibrosis induces wide expression of COX-2 in the regenerating metaplastic epithelium.
- COX-2 is expressed at higher levels in orbital fibroadipose tissues of Graves' ophthalmopathy (GO) cases; this showed a positive correlation with increasing severity of orbital disease suggesting relation with COX-2 expression & orbital inflammation in G
- This review covers factors influencing COX enzyme activity, the role of their products in the development and maintenance of pain and discusses recent safety concerns of COX-2 inhibitors.
- These results suggest that the COX-2-PGE(2) pathway may be involved in IL-8 production in gastric epithelial cells.
- The first evidence of the presence of COX-2 in mature neutrophils in bone marrow. Its expression varied with stage of differentiation. It may have a role in residual hematopoiesis in myelodysplastic marrow.
- These results suggest that in bone fibroblasts elevated extracellular Ca(2+) may enhance COX-2 expression via the activation of ERK1/2, p38 MAPK, and JNK through CasR.
- COX-2 expression and mPGES-1 expression are co-ordinately up-regulated in lower segment myometrium with term labour.
- COX-2 turnover appears to depend upon glycosylation of the 72kDa glycoform.
- COX-2 and beta-Catenin may have roles in regulating intracellular Survivin levels in mouse and human colon cancer
- alteration in monocyte COX mRNA expression as well as monocyte COX-2 after lipopolysaccharides in type 1 diabetic patients and their nondiabetic twins.
- Findings indicate that IL-1beta-induced Cox-2 expression in human myometrial smooth muscle cells is dependent on the action of atypical PKCs, through stimulation of the activity of NF-kappaB.
- These are the first results to provide evidence that a combined association implicating a MEK inhibitor (U0126) and diosgenin is the most effective in inducing very strong apoptosis with down-regulation of COX-2 expression and activity in human RA FLS.
- Inherited polymorphisms in cyclooxygenase (COX)-2 may confer susceptibility to colorectal cancer in Han Chinese.
- glycodelin and COX-2 might play important roles in promoting neovascularization and cell proliferation in the establishment of endometriosis
- invasive human breast cancer cells that over-express COX-2 develop vascular channels, non-invasive cell lines that express low levels of COX-2 did not develop such channels.Celecoxib or COX-2 siRNA suppressed vascular channel formation.
- NLS (KKFKKY; aa307-312) is located within the cytoplasmic tail of the AT(1A) receptor and that nuclear localization of the receptor corresponds with specific activation of transcription for the COX-2 gene PTGS-2.
- Possible influence of the COX-2 C8473T SNP in Parkinson's disease, although it only seems to be of importance in men.
- The up-regulation of COX-2 gene and down-regulation of COX-1 gene expression suggests that acetaminophen may result in changes in COX-derived prostanoids with repeated doses.
- Data suggest that the nascent intracellular form of cyclooxygenase-2 may undergo limited proteolysis to attain full catalytic capacity.
- Understanding of COX-2 downstream signaling pathways in colon cancer cell lines that promote tumor progression is crucial for the development of novel therapeutic strategies.
- PPARdelta induces COX-2 expression and the COX-2-derived PGE(2) further activates PPARdelta via cPLA(2)alpha. which forms a growth-promoting signaling that may play a role in hepatocarcinogenesis.
- over-expression of cyclooxygenase 2 is associated with breast cancer
- women homozygous for the T allele at rs5275 had a 20% lower risk of breast cancer than those homozygous for the C allele (odds ratio 0.80, 95% confidence interval 0.66 to 0.97)
- Stretch of the amnion, on onset of labor, may contribute to increased expression of COX-2.
- Increasing COX-2 expression in Barrett's metaplasia is significantly associated with a change in the local inflammatory reaction, but not during further progression through dysplasia to cancer
- This study suggested that PTGS2 gene was a predisposition gene and arachidonic acid metabolism might be involved in the pathogenesis of AD.
- Our present study demonstrated a significant overexpression of COX-2 at the mRNA and protein level in the Barrett's epithelium
- Analysis of gene expression demonstrated a significant elevation in expression of COX-1 and COX-2 mRNA in endometrium obtained from women with heavy MBL (menstrual blood loss) when compared with endometrium obtained from women with normal MBL.
- correlation between COX-2 and polo-like kinase-1 in a malignant prostate tumor
- Most tumor cells stained positive for COX-2 protein.
- Results suggest that expression of microsomal PGES in addition to COX-2 plays a role in increasing PGE(2) production in endometriosis.
- human aortic smooth muscle cells prostacyclin 2 synthase(PGIS) gene transfer reduced peroxisome proliferator-activated receptor delta(PPAR-delta) expression and inhibited neointimal formation after balloon injury
- Polymorphisms in COX-2 is associated with basal cell carcinoma
- Patients with tumor lacking cyclooxygenase-2 expression before chemoradiotherapy are more likely to demonstrate good response to treatment.
- Relatively few individuals expressed the intron 1-retaining COX-1b variants (COX-1b1, -1b2, and -1b3) at any time point, and when expressed, these variants were in very low abundance.
- Cox-2 positive cases had aggressive histology in in non-Hodgkin's lymphomas
- Kinin B1 and B2 receptors synergistically potentiate IL-1- and TNFalpha-induced PG biosynthesis in osteoblasts by a mechanism involving increased levels of COX-2, resulting in increased RANKL.
- COX-2 increases breast cancer invasion through the PKC/IL-8/uPA pathway.
- production of prostacyclin in a human follicular dendritic cell line is controlled by the regulation of upstream COX-2
- These data demonstrate that IGF-I induces COX-2 expression in human ovarian cancer cells, which is mediated by three parallel signaling cascades--PI3K, MAPK, and PKC pathways that differentially regulate COX-2 expression.
- G-CSF and GM-CSF might accelerate tumor progression by directly regulating COX-2 expression, independently of an autocrine mechanism.
- We have found the COX-2 G-765C polymorphism to be a risk factor for incident stroke in African-Americans
- Study demonstrates correlation between over expression of NF-kappaB and COX-2 in early precancerous stages of development of oral cancer and sustained elevation down the tumorigenic pathway.
- Screening of the proximal 5' regulatory region and genotyping of -765G>C and -62C>G showed that polymorphisms in this COX-2 region are unlikely to be involved in MS susceptibility.
- Data show that regulation of HuR via protein kinase C alpha-dependent phosphorylation emphasizes the importance of posttranslational modification for stimulus-dependent HuR shuttling.
- Results show for the first time acetylation via selective degradation of histone deacetylase 1, and that recruitment of histone acetyltransferase plays an important role in diesel exhaust particulate matter-induced expression of the cyclooxygenase-2 gene
- No association of COX-2 and inducible nitric oxide (NOS2) polymorphisms with cervical cancer is found in Korean women.
- Vulvar cancer in elderly patients may be associated with inflammation, and thus with increased COX-2 expression.
- H. pylori induces COX-2 expression, which is mediated by both activation and expression of PAR-2 in gastric epithelial cells
- In this test set, cyclooxygenase 2 and Caspase 3 seem to be immunohistochemical markers with prognostic significance for vulva cancer.
- COX-2 expression in MCF10A breast epithelial cells confers a premalignant phenotype that includes enhanced genomic instability and altered cell-cycle regulation.
- epiregulin, COX2, and MMP1 and 2 collectively facilitate the assembly of new tumour blood vessels, the release of tumour cells into the circulation, and the breaching of lung capillaries by circulating tumour cells to seed pulmonary metastasis
- Results demonstrate that COX-2 physically interacts with the COP9 signalosome and its degradation is regulated by the COP9 signalosome.
- Vasoactive intestinal peptide stimulated both COX-2 mRNA and protein expression in a faster manner as prostate cancer stage progressed.
- Down-regulation of cyclooxygenase-2 by celecoxib is associated with decreased expression of cyclooxygenase-2, pAkt and carbonic anhydrase, and eventual radiation sensitization, which is a phenomenon that may have clinical usefulness.
- PRKCD-mediated CREB activation regulates ghrelin-induced COX-2 expression and dinoprostone production in colonic epithelial cells.
- results suggest that COX-2 expression may be differentially regulated among subdivisions of the hippocampus and that elevated COX-2 expression in the CA1 of Alzheimer's disease (AD) brains may be associated with AD pathology and thus cognitive dysfunctio
- n-3 and n-6 polyunsaturated fatty acids increase PPARG activity is necessary for cyclooxygenase-2 induction in a human keratinocyte cell line.
- Inherited polymorphisms in arachidonic acid-metabolizing enzymes, which result in heightened gene expression or enzymatic activity, may confer host susceptibility to esophageal squamous cell carcinoma.
- Polymorphisms predicted to alter function in prostaglandin E2 synthase.
- Haplotypes A-1195G-765T8473 and A-1195C-765T8473 variants of COX-2 were significantly associated with breast cancer risk
- Genetic variation in PTGS1 and PTGS2 may be important risk factors for the development of cardiovascular disease events.
- Cox2 may not be responsible for cell proliferation in ovarian tumors.
- Identification of PSF, p54(nrb), PTB, and U1A as proteins specifically bound to the COX-2 polyadenylation signal upstream sequence elements .
- After Hp eradication, CDH1, p16, and APC methylation significantly decreased while COX2 methylation completely disappeared.
- These data show that silencing of COX-2 abolishes the metastatic potential of MDA-MB-231 cells in vivo.
- COX-2 expression correlates with VEGF expression and might be a useful prognostic factor for more frequent tumor recurrence in esophageal squamous carcinoma patients undergoing neoadjuvant chemoradiotherapy.
- COX 2 existed in pterygium. COX 2 may play role in pterygium formation.
- participates in placentation through EVT invasion by up-regulating PGE2 production and PGE2 receptor expression in first trimester extravillous trophoblasts
- The majority of meningioma cases studied were positive for COX2 overexpression.
- COX-2 is expressed at high levels in high grade osteosarcomas
- COX-2 is highly expressed in lobular in situ neoplasia, supporting a role for this protein in the early stage of breast carcinogenesis, representing the rationale for using COX-2 selective inhibitors in the earliest stages of breast cancer.
- Cyclooxygenase-2 impairs treatment effect of radiotherapy for cervical cancer by inhibition of radiation-induced apoptosis.
- Signaling pathways involved in PTGS2 induction by hepatocyte growth factor in non-small-cell lung carcinoma are reported.
- COX-2 overexpression was significantly correlated with depth of invasion, tumor stage and survival in esophageal squamous cell carcinoma.
- COX activity appears to be required for efficient mouse hepatitis virus replication, providing a potential target for anti-coronaviral therapy
- Results indicate that COX-2 is highly up-regulated during both normal and stress-induced fibroblast senescence and contributes to the establishment of the senescent characteristics.
- tetrahydrobiopterin-induced COX-2 expression is responsible for dopamine oxidation, leading to the preferential vulnerability of dopaminergic cells in Parkinson's disease
- dexamethasone reduces vasoconstriction to electrical field stimulation in rat mesenteric arteries from spontaneously hypertensive rats by decreasing COX-2 expression, decreasing the smooth muscle TXA(2) release induced by alpha-adrenoceptor activation
- data demonstrated that chronic inflammation appeared to play roles in induction of CCAAT/enhancer-binding protein beta expression in prostate epithelium which was associated with increased Cyclooxygenase-2 expression and androgen receptor downregulation
- E-prostanoid receptors 2-4, but not 1, transactivated the epidermal growth factor receptor, through tumor necrosis factor-alpha converting enzyme.
- PTGS2.8473 polymorphism is associated with asthma, atopy and lung function but not plasma IgE in Chinese children.
- COX-2 common variants -765G-->C and -1195A-->G appear to be associated with risk of nonmelanoma skin cancer, although in different ways in the squamous cell skin carcinoma and basal cell carcinoma subgroups
- COX-2 CA-haplotype is a risk factor for development of esophageal adenocarcinoma.
- Results suggest that the cytoplasmic overexpression of HuR is associated with uterine cervical carcinomas with aggressive clinicopathologic features and that HuR might contribute to the stabilization of COX-2 mRNA in some uterine cervical carcinomas.
- Data support that there are significant differences between EGFR and COX-2 expressions in the 3 different histogenetic types of cervical cancer.
- A fetal polymorphism in the COX-2 gene influences the occurrence of placental malperfusion and ischemia, which may be of sufficient severity to promote or allow the development of intrauterine growth retardation.
- low density lipoprotein (LDL) that had been denatured by freeze-thawing or oxidized LDL might be involved in the COX-2 induction
- The PRBC group had a significantly different expression profile included up-regulation of the prostaglandin-endoperoxide synthase-2. PRBCs activate inflammatory genes in circulating leukocytes.
- Up-regulation of Rac1 by epidermal growth factor mediates COX-2 expression in recurrent respiratory papillomas.
- Rsults suggest that COX-2 expression might play an important role in the progression of colorectal cancer.
- Overall, our results suggest that certain alkamides derived from E. angustifolia roots may contribute to the pharmacological action of the herbal extract by inhibiting COX-2-dependent PGE2 formation at sites of inflammation.
- the transcriptional activity of the COX-2 gene in colorectal cancer cells and the identification of regulatory promoter elements
- Our findings suggest that variation in COX2 is associated with prostate cancer risk.
- Results show co-expression of cyclooxygenase-2 and prostaglandin E2 receptors EP1, 2 and 4 in non-small cell lung cancer cells concomitant with the synthesis of PGE2.
- study demonstrated that the gene expression of cyclooxygenase-2 and SCD diminished in the chronic phase of Graves'ophthalmopathy in parallel with a decrease in clinical activity score
- EGFR activation in malignant gliomas can transcriptionally activate COX-2 expression in a process that requires p38-MAPK and Sp1/Sp3
- COX-2, MMP-2 and MMP-9 were expressed in a high percentage of primary endometrial carcinomas and their expressions may be associated closely with parameters of tumor aggressiveness.
- Expression might be addressed as a new prognostic tool in the clinical management of oral squamous cell carcinoma.
- Inhibition of COX-2 may reduce the development of postoperative adhesions by preventing the formation of the adhesion phenotype.
- Results indicate that gp120 induces COX-2 transcription through NF-kappaB activation in astrocytoma cells.
- YKL-40 release by intervertebral disc culture may better clarify its role in the pathophysiology of discal degeneration and inflammation and its relationships with COX-2 and NO in disc tissue culture.
- GS-HCl inhibits COX-2 activity by preventing COX-2 co-translational N-glycosylation and by facilitating COX-2 protein turnover during translation in a proteasome-dependent manner
- polymorphisms are unlikely to influence colorectal adenoma recurrence and cannot be used to identify individuals who derive benefit from aspirin interventio
- These results demonstrate for the first time that PLD1 and PLD2 isozymes enhance cobalt chlorde-induced COX-2 expression through differential signaling pathways in astroglioma cells.
- Data show that the Ca2+-dependent type IV cytosolic phospholipase A2 (cPLA2) is pivotally involved in the COX-2-mediated generation of PGE2 in response to a calcium ionophore.
- The major subtypes of renal epithelial neoplasms display differential aberrant CDH1, PTGS2, and RASSF1A promoter methylation levels. This gene panel might contribute to a more accurate discrimination among common renal tumors.
- The expression of cyclooxygenase-2 COX2) was significantly higher in esophogeal squamous cell neoplasm than in non-tumorous tissue.
- These data suggest that the COX-2-dependent pathway appears to assist TMT-induced degeneration of CA1 pyramidal cells but not CA3 pyramidal cells in a corticosterone-independent manner.
- This study demonstrates a strong positive relationship between COX-2 and aromatase mRNA expression, and lends further support to the hypothesis that COX-2 is an upregulator of aromatase in breast tissue
- VEGF, MMP2, 7 and 9, and COX-2 expression is related to progression of advanced uterine cervical cancer in young women
- High frequency of expression in central nervous system lymphomas may be associated with tumorigenesis may lead to futural therapeutic trials.
- COX-2 is expressed and enzymatically active in myocytes of skeletal muscles and hearts of humans.
- mechanisms leading to microglial COX-2 expression as well as its potential implication in prion disease pathogenesis remain to be established--REVIEW
- Findings suggests that COX-2 might play a role in pathogenesis of atheroscleros and modulation of inflammatory process involved in plaque stability, and COX-2 may have proinflammatory enzyme properties.
- Slow transit constipation is due to abnormal levels of COX1/2 and prostaglandins, probably caused by overexpression of progesterone receptors in colonic smooth muscle.
- mechanism of COX-2 protein induction expression in PMN is substantially different from that operative in mononuclear phagocytes, which is highly dependent on transcriptional regulation
- COX-2 and iNOS was significantly higher in chronic fatigue syndrome patients than in normal controls.
- High concentrations of specific COX2 inhibitors inhibited proliferation of esophageal tumor cell lines.
- Cytoplasmic beta-catenin is associated with COX-2 overexpression, supporting the role of cytoplasmic beta-catenin in stabilizing PTGS2 (COX-2) mRNA.
- The switching of linoleic acid metabolism by reversal of the expression of 15LOX-1 and COX-2 is associated with acquisition of malignant potential in colonic neoplasia.
- Metabolism of endocannabinoids by the endothelial cell COX-2 coupled to the prostacyclin (PGI(2)) synthase activates the nuclear receptor peroxisomal proliferator-activated receptor delta, which negatively regulates the expression of tissue factor.
- AhR activation and COX-2 overexpression likely represent a mechanism of resistance to apoptosis in lymphoma cell lines that might be relevant for the development of lymphoma in vivo.
- COX-2 (-1195G) is likely to result in a better non-small cell lung cancer response to vinorelbine (nonsignificant).
- COX-2 is localized within caveolae compartment and colocalized with CAV-1 protein in lobular intraepithelial neoplasia of the breast.
- We report that arachidonic acid lipid hydroperoxide metabolites of 5-, 12-, 15-lipoxygenase-1, and cyclooxygenase-2 oxidize the 2-Cys-peroxiredoxins 1, 2, and 3 to their sulfinic and sulfonic forms.
- these results demonstrate that vGPCR induces expression of COX-2 and PGE2 that may mediate the paracrine effects of this key viral protein in KS pathogenesis.
- COX-2 probably mediates inflammatory reaction in myocardial infarction. COX-1 and COX-2 are associated with the healing processes and scar formation after myocardial infarction.
- CDX2 inhibits transcription of Cox-2 by interfering with the binding of NF-kappaB on the NF-kappaB binding site.
- Three classes of inflammatory repressors act synergistically in modulating PAF-induced up-regulation of COX-2, TNFalpha, and PGE(2) by quenching oxidative stress or inflammatory signaling, resulting in increased HN cell survival.
- RU486 attenuates the activation of ERK1/2, decreases the expression of COX-2, and affects PGE2 production by inhibiting hCG-induced COX-2 expression.
- In healthy volunteers, COX-2 inhibition inhibited systemic PGE2/PGI2 synthesis and stimulated TXB2 release from activated platelets.
- We report that Bordetella persussis ACT ( adenylate cyclase toxin) induces COX-2 in HEK293T cells expressing Mac-1.
- transactivation of the COX-2 promoter and MAPK pathway by cholecystokinin-2/gastrin receptor
- Breast cancer progression is associated with the accumulation of glucocorticoid receptor in the cytoplasm of tumoral cells and the decrease of COX-2 expression.
- The experiments presented here demonstrated that COX-2 transfection of a TGF-beta-sensitive cell line abrogates the growth inhibitory effects of TGF-beta.
- Together, our results demonstrated that COX-2 expression could be induced by vanadium pentoxide in NFAT-dependent way and played an anti-apoptotic role in Beas-2B cells.
- PAR2 up-regulates cyclooxygenase-2 expression via an ERK1/2-mediated activation.
- microparticles up-regulate the production of PGE(2) in synovial fibroblasts by inducing COX-2 and mPGES-1 in rheumatoid arthritis
- These results suggested that tumor-produced COX-2, which was associated with inhibiting apoptosis and promoting angiogenesis, provided additional prognostic information in endometrial cancer patients.
- COX-1 and COX-2 are constitutively expressed at relatively high levels in human patellar tendon and are likely targets of COX-inhibiting drugs at rest and after physical activity.
- Jak2 ordinarily dampens and limits the duration of the PGHS-2 induction by IL-1beta.
- COX-2 mRNA and proteins were significantly reduced by up to 80% on day 2 after COX-2 siRNA transfection to the gastric cancer cell line.
- LTD(4) promotes formation of an atherosclerosis-protective and anti-thrombotic eicosanoid by markedly up-regulating EC cyclooxygenase-2 (COX-2).
- large study of five PTGS2 SNPs does not support a strong association between PTGS2 variants and prostate cancer risk in non-Hispanic white men
- Tumor COX-2 expression portends a poor prognosis for patients with resected adenocarcinoma of the pancreas, particularly in tumors > or =3 cm.
- Rho-GDI beta has two roles: one that suppresses tumor progression by inhibiting migration and the other that stimulates it by enhancing Cox-2 expression
- There was a statistically significant correlation between COX-2 immunoreactivity and the cytoplasmic HuR expression level in laryngeal squamous cell carcinoma.
- COX-2 has the ability to enhance iNOS-induced cPLA(2)alpha S-nitrosylation and maximal PG synthesis is achieved by the synergistic interaction among iNOS, cPLA(2)alpha, and COX-2
- Stromal myofibroblasts surrounding colon adenocarcinomas are an important source of VEGF and COX-2 production.
- For T-cell non-Hodgkins Lymphoma, the COX2 rs2745557 A-allele conferred a 2.2-fold elevated risk
- Inhibition of COX-2 decreases endometriotic epithelial and stromal cell survival, migration, and invasion in humans.
- COX-2 expression was increased in women with endometriosis as compared with control endometrium.
- Cyclooxygenase-2 and VEGF were closely correlated with each other, and both of them appear to play a role in the angiogenesis of ovarian endometriosis.
- Alternative splicing of platelet COX2 mRNA after coronary bypass grafting may be a posttranscriptional mechanism opposing transactivation of COX-2. Prevents COX-2-dependent thromboxane synthesis in the platelet, increasing the likelihood of thrombosis.
- IL-17A enhances the expression of cyclooxygensase-2 and IL-8 and the proliferation of endometriotic stromal cells. IL-17A may play a role in the development of endometriosis.
- Data show that MCP-1 has a synergistic effect on COX-2 and CCR2 protein expression in CD40L-stimulated HUVECs and stimulates VEGF production in these cells.
- COX-2 expression is dependent on calcium and protein kinase C
- HIV-1 Tat was able to induce COX-2 and PGE2 synthesis in astrocytic cells through an NFAT/AP-1-dependent mechanism.
- we analyzed the signal transduction and COX-2 expression in endometrial cancer cells
- LPS-activated monocytes suppress T cell immune responses and induce FOXP3 expression in resting CD4+CD25- T cells through a COX-2-PGE2-dependent mechanism.
- Cyclooxygenase 2 expression was significantly associated with lymph node metastasis.
- Bupivacaine stimulates COX-2 gene expression after surgery, which is associated with higher PGE2 production and pain after the local anesthetic effect dissipates.
- the relation of COX-2 polymorphisms (-1195G>A, -765G>C and 8160A>G) to colorectal adenomas in a case-control study of male officials in the Self Defense Forces (SDF).
- Increased expression of COX-2 and survivin in ovarian cancer is associated with adverse clinicopathologic parameters, including reduced survival.
- COX-2 overexpression in glottic cancer was associated with increased overall mortality and an increased risk of second primary cancers in head and neck cancer patients during the early follow-up period
- The results of the study suggest that the -765G to C polymorphism of the COX-2 gene is associated with a decreased risk for periodontitis in Taiwanese, especially in AgP. However, the biological meaning needs further investigation.
- Osteopontin, cyclooxygenase-2 and vascular endothelial growth factor synergically promote angiogenesis and metastasis in gastric cancer.
- Cox-2 is heterogeneously expressed in glioblastomas without a significant association with microvessel density
- COX-2 may up-regulate VEGF-C expression and thus promote lymph node metastasis via lymphangiogenesis pathway in human breast cancer.
- 15-Deoxy-Delta12,14-prostaglandin J2 produced by COX-2 overexpression may function as a positive regulator of COX-2 in human breast cancer MCF-7 cells.
- COX-2 expression is decreased in breast cancer cell lines and cancer specimens as compared with normal mammary epithelial cells.
- COX-2 immunostaining does not distinguish dermatofibroma from dermatofibrosarcoma protuberans.
- the subcellular localization of HuR is deregulated in a subset of prostate carcinomas, and that this deregulation is linked to an altered expression of the tumorigenic COX-2 protein as well as to an adverse patient prognosis
- second pathway for COX-2 protein degradation is initiated by substrate-dependent suicide inactivation
- Data conclude that the proximal 1000 bp region is involved in PGHS-2 promoter regulation in term amnion.
- upon stimulation with the same upstream signals, different downstream intracellular pathways regulate PTGS2 and PGDH mRNA expression
- results suggest that the polymorphisms examined in COX1 and COX2 do not affect the risk of gastric cancer
- PUFAs undergo biotransformation by COX-2 to lipid mediators that modulate tumor angiogenesis, which provides new insight into the beneficial effects of omega-3 PUFAs.
- Strong COX-2 overexpression in colorectal carcinogenesis is more common in non-serrated adenomas than in hyperplastic polyps and serrated polyps. Regardless of serration, COX-2 overexpression is frequent in colorectal adenocarcinomas.
- nontypeable Haemophilus influenzae induces COX-2 and PGE2 expression in a p38 MAPK and NF-kappa B-dependent manner through TLR2 in lung epithelial cells in vitro and lung tissues in vivo
- Hepatocyte growth factor induces gene transcription of COX-2 in human bronchial epithelial cells.
- In breast cancer patients treated with CS+RT, COX-2 expression is associated with younger age, larger tumor size, worse local control, distant metastasis, and worse overall survival.
- Ultrasound increased COX-2 expression in osteoblasts via the LKB1/AMPKalpha1/p38/IKKalphabeta and NF-kappaB signaling pathway.
- Results describe the cyclooxygenase (COX) and 5-lipoxygenase (5-LOX) selectivity of COX inhibitors.
- In early stage oral squamous cell carcinomas, most tumours did not express COX-2 at the invasive front.
- Posttranslational modification of HuR by protein kinase Cdelta represents an important novel mode of HuR activation implied in renal COX-2 regulation
- COX-2 was found to be more strongly expressed in poorly-differentiated than in moderately/well-differentiated hypopharyngeal carcinomas.
- Increased transgenic COX-2 expression significantly enhances basal synaptic transmission and augments long-term potentiation in the hippocampus.
- Data show that vitamin C suppresses proliferation of the human melanoma cell line SK-MEL2 via the down-regulation of IGF-II production and IGF-IR expression, which is followed by the activation of p38 MAPK and the inhibition of COX-2 expression.
- Lewy body nigral COX-2 mRNA expression does not correlate with dopaminergic neurodegeneration; changes observed are probably due to concomitant Alzheimer disease.
- the COX-2 -765 G allele promoter polymorphism is significantly associated with gastric cancer
- Data show that prostag;andins E2 and F2alpha can mobilize inositol 1,4,5-trisphosphate, induce ERK1/2 phosphorylation and induce cyclooxygenase-2 expression via the FP receptor.
- CCR7 and the EP2/EP4 receptor signaling pathway are down-stream targets for COX-2 to enhance the migration of breast cancer cells toward LECs and to promote lymphatic invasion
- Report COX2 dependent/independent antitumor effects of COX2 inhibitors on colon tumor cells.
- Defining hyaluronan-dependent cyclooxygenase-2/prostaglandin E(2)-associated signaling pathways will provide a platform for developing novel therapeutic approaches for colon cancer
- -765G > C COX-2 polymorphism with or without H pylori could be a marker for genetic susceptibility to gastric adenocarcinoma.
- investigation of whether COX-2 overexpression in atypical hyperplasia is associated with risk of subsequent breast cancer; COX-2 appears to be a biomarker that further stratifies breast cancer risk among women with atypia
- Data show that substance P receptors are found on polymorphonuclear cells, and that interaction with nanomolar concentrations of substance P induces cycloxygenase-2 expression.
- The COX-2 8473 C allele is a potential genetic marker for susceptibility to esophageal adenocarcinoma.
- COX-2 -765G>C polymorphism not associated with an increased risk of colorectal cancer, but may modifiy risks associated with smoking and higher body mass index.
- expression in oral cancer was found to be independent of grade of tumor and stage of disease
- Up-regulation of COX-2 protein synthesis in human thyroid diseases does not appear to be of clinical significance.
- Forced COX-2 expression in SV-HUC immortalized urothelial cells contributes to increased PGE2 production and increased invasion through Matrigel.
- Signaling network regulating shear-induced COX-2 expression and inflammation may provide insights to optimize conditions for culturing artificial cartilage in bioreactors and for developing therapeutic interventions for arthritic disorders.
- MCP-1 and CD40L had a synergistic effect on COX-2 expression and subsequent VEGF production in gastric cancer.
- Stromal expression of COX-2 (cyclooxygenase 2), was significantly higher in premenopausal endometrial polyps compared to postmenopausal polyps
- There is a possible protective influence of the C allele for 6365T-->C and for -899G-->C in the cyclooxygenase-2 (COX-2) gene rheumatoid arthritis in Koreans. The radiologic severity of RA was not associated with COX-2 polymorphisms.
- longer progression-free survival with high-tumor COX-2 expression suggests that trials of EGFR and COX-2 inhibitors may be warranted in this patient subse
- This study singled out PTGS2 as a promising bladder cancer susceptibility gene
- Data show that the COX-2 polymorphism was not associated with MI. Our data suggest that COX-2 may be involved in plaque growth.
- COX-2 expression is overexpressed in the majority of rectal cancers treated with radiotherapy and likely plays a role in local relapse.
- Aceetylsalicylic acid-dependent inhibition of hepatitis c virus replication is due in part to inhibition of COX-2.
- Gastrin differentially induces COX-2 and IL-8 expression at the transcriptional and posttranscriptional levels by PI3K and p38 mitogen-activated protein kinase pathways, respectively.
- STAT3 activation mediates COX-2 expression and ischemic tolerance.
- Oleanolic acid and its analog inhibited COX-2 and induced apoptosis in human colon HT-29 cancer cells.
- Human neutrophil peptides upregulate expression of COX-2 and endothelin-1 by inducing oxidative stress.
- UVB irradiation regulates COX2 mRNA stability through AMPK and HuR in human keratinocytes.
- High COX-2 expression is associated with lung neoplasms
- in lupus nephritis COX-2 and monocytes/ macrophages but not COX-1 isoform are involved in the inflammatory process.
- This study associates COX-2 epithelial expression with a number of colorectal adenoma characteristics that convey an increased risk of malignant transformation.
- Found that COX-2 expression was significantly higher in earlier stages of gastric cancer.
- COX2-PGE2 pathway may be involved in H. pylori-associated Urokinase-type plasminogen activator (uPA) and its receptor induction
- A role for COX-2 as a predictor of adverse effects of tamoxifen in breast cancer patients.
- a polymorphism in LD with variants affecting the expression of the PTGS2 gene are associated with susceptibility to knee OA in five independent populations and highlight the importance of inflammatory pathways in OA pathogenesis
- Results show that GPx2 by compartmentalized removal of hydroperoxides silences COX-2 activity and suppresses PGE(2)-dependent COX-2 and mPGES-1 expression.
- Study of Australian Caucasians suggests that the -1195G>A polymorphism appears to be associated with asthma, and in particular with mild asthma.
- Wogonin inhibits phorbol myristatae acetate-induced COX-2 gene expression in a lung cancer cell line.
- COX2 expression in MCF7 breast cancer cells induced genomic instability, BCL2 expression, and doxorubicin resistance, thus making them significantly more tumorigenic.
- The results suggest that COX-2 does not appear to mediate the development of liver fibrosis.
- C/EBP beta overexpression significantly upregulated promoter activities of IL-8, COX-2, and anti-apoptotic Bfl-1 genes in prostate cancer cells.
- C allele of the COX2.3050G>C polymorphism is associated with systemic sarcoidosis
- Transcription of the invasion suppressor, CRMP-1, is reciprocally regulated at the promoter region by C/EBPalpha and Sp1.
- Data show that Mexico City dogs exhibit frontal white matter upregulation of two important inflammatory genes: COX2 and IL1beta, compared to age-matched control dogs from a low polluted area.
- 7-hydroxyandrosterone decreased COX2 expression.
- Report the differential effects of triptolide and tetrandrine on activation of COX-2, NF-kappaB, and AP-1 and virus production in dengue virus-infected human lung cells.
- VEGF expression was statistically correlated to c-fms and COX-2 expression in high-grade CIN.
- Report the long-term effect of Helicobacter pylori eradication on COX-1/2, 5-LOX and leukotriene receptors in patients with a risk gastritis phenotype--a link to gastric carcinogenesis.
- The increase in COX2 expression and the activation of Erk1/2 regulated by Cot are essential for the induction of cell migration.
- We found that the A allele of PTGS2 rs2745557 was preferentially transmitted in ASDs (p < 0.01) and that the GAAA haplotype was significantly associated with autism spectrum disorders (p < 0.01).
- RNA interference technology was employed to downregulate endogenous gene COX-2 expression in laryngeal carcinoma cells and the phenotypical changes were analyzed.
- Most Merkel cell carcinomas express COX-2; its expression is related to one parameter of aggressive behavior--a high mitotic rate--but not to any others.
- COX-2 is an important survival factor mediating the oncogenic actions of hepatitis B virus X protein.
- Transfected into mice, overexpresssion promotes chemical-induced gastric carcinogenesis.
- Data show that particulate matter induces cyclooxygenase-2 expression and IL-6 release through both a reactive oxygen species (ROS)-dependent NF-kappaB pathway and an ROS-independent C/EBPbeta pathway in human bronchial epithelial cells in culture.
- Lysophosphatidic acid might regulate VEGF-C and lymphatic marker expression in endothelial cells, which contributes to endothelial cell tube formation in vitro and in vivo, thus facilitating endothelial cell participation lymphangiogenesis.
- COX-2 gene methylation was more common in subepithelial lymphocytes than in adjacent epithelial or stromal cells in both grades of dysplasia and in foci of invasive cancer
- EGFR activation induces COX-2 expression through PI-3K and/or p38MAPK pathways
- NMDA neurotoxicity is mediated by S-nitrosylation/activation of COX-2
- In human chondrocytes, the inhibition of complexes III and V of the mitochondrial respiratory chain induces an inflammatory response, which could be especially relevant in relation to COX-2 and PGE(2) production.
- Data show that tissue-specific COX-2-dependent prostaglandins exert an efficient protection against acute liver injury by an antiapoptotic/antinecrotic effect and by accelerated early hepatocyte proliferation.
- VEGF production is COX-2 dependent in NSCLC cells expressing COX-2; IL-8 production is COX-2 independent in both NSCLC and SCLC cells
- overexpression of COX-2 increases the intracellular production of MRP1 and MRP2 and causes drug resistance to cisplatin
- COX-2 expression in Ewing sarcoma may not be directly related to mRNA stabilization by HuR. However, a correlation between COX-2 expression and nuclear HuR expression through indirect mRNA stabilization can be suggested.
- Platelets contained cyclooxygenase-2 pre-mRNA, which also was spliced and translated after LPS stimu
- Data show that COX-2 blockade enhances endothelial cell-dependent increases in osteoblast differentiation, that this effect was reversed by exogenous PGH(2), and that exogenous VEGF did not influence EC-dependent OB differentiation under these conditions
- Cox-2 was ubiquitously expressed in all cases of Wilms' tumor
- despite the presence of COX-2, COX-1 is functionally predominant in the airways and explains clinical observations relating to drug specificity in patients with aspirin-sensitive asthma.
- gradually increased COX-2 expression might contribute to the dendritic cells functional defect.
- Predominant expression of COX-2 in the carcinomas of intestinal type and its precursory lesions.
- Glycine-extended gastrin induced signalling involves a JAK2/PI3-kinase/Akt/NF-kappaB sequence leading to COX-2 transcription.
- Cyclooxygenase-2 allele C is associated with a reduced time interval from labor induction to delivery.
- The reduced expression of COX-2 in CIN specimens may suggest that clue cells interfere with the inflammatory component of the carcinogenic process that lead to CIN.
- bile acid induces an increase in the gene expression of COX-2 via the sequential transcriptional induction of SHP and CDX1 in precancerous lesions of human gastric cancer
- COX-2 promotes colon tumor progression, but not initiation, and it does so, in part, by activating EGFR and Akt signaling pathways
- Proline oxidase, a p53-induced gene, targets COX-2/PGE2 signaling to induce apoptosis and inhibit tumor growth in colorectal cancers
- the results from recent studies suggest that Tpl2/Cot and COX-2 could be prognostic factors in breast cancer [review]
- COX-2 expression correlated inversely with disease-specific survival in patients with osteosarcoma lung metastases.
- COX-2 induces cell viability and migration, & promotes the proliferation of CAOV-3 cells via the PI3-kinase/Akt signal pathway.
- altered expression of PGE(2) enzymatic pathways may promote the cervical carcinogenesis by favouring (pre)cancer immunotolerance.
- Enhancement of PGD2 production through COX-2 and LPGDS by USF1 in human brain-derived TE671 cells under serum starvation are reported.
- HuR plays a role in tumor progression in mesothelioma and that COX-2 may be a target of its activity
- PGE(2) via EP(4) activates the EGFR --> ERK1/2 --> Egr-1 pathway, leading to increased Id-1 transcription and cell invasion
- HNRNP K and microRNA-16 have roles in cyclooxygenase-2 RNA stability induced by S100b, a ligand of the receptor for advanced glycation end products
- role of the COX-2 promoter region in contributing to the development of betel-related oral squamous cell carcinoma.
- Dose-dependent effects of rosmarinic acid on activator protein 1 activation of cyclooxygenase 2 in normal and neoplastic cells lines is reported.
- COX-2 silencing resulted in loss of several functional phenotypic characteristics associated with malignancy in poorly differentiated MDA-MB-231 breast cancer cells; data highlight the functional role of COX-2 in pathways that mediate increased malignanc
- These findings in conjunction with findings in other populations of African descent might suggest a common causal variant for prostate cancer in COX-2, or a variant in a nearby gene.
- Common polymorphisms of cyclooxygenase-2 and prostaglandin E2 receptor and increased risk for acute coronary syndrome in coronary artery disease.
- The pro-inflammatory alleles of COX-2 and 5-LO were overrepresented in MI and under-represented in centenarians whereas age-related controls displayed intermediate values
- R(+)-methanandamide-induced apoptosis of human cervical carcinoma cells involves a cyclooxygenase-2-dependent pathway.
- PTGSw2 gene expression was significantly higher in colorectal cancer patietnts than in healthy volunteers.
- Transgenic expression of cyclooxygenase-2 in hepatocytes accelerates endotoxin-induced acute liver failure.
- IL-1beta-induced COX-2 expression strongly at both protein & messenger ribonucleic acid levels in U87MG glioma cells and astrocytes.
- Allelic variants of the COX-2 gene significantly influence the risk of colorectal adenoma development in the African American population.
- Polymorphisms in COX-2 and EGFR may be useful independent molecular markers to predict clinical outcome in patients with metastatic colorectal cancer treated with single-agent cetuximab
- Data show that GPx2 inhibits malignant characteristics of tumor cells, migration and invasion, obviously by counteracting COX-2 expression but is required for the growth of transformed intestinal cells and may, therefore, facilitate tumor cell growth.
- Although COX-2-765G>C and IL-6-174G>C polymorphisms were associated with inflammation, consuming a Mediterranean diet either supplemented with virgin olive oil or nuts reduced the concentration of inflammation markers.
- Naturally occurring modulators of the aryl hydrocarbon receptor (AhR) such as 3,3'-diindolylmethane (DIM) may be effective agents for dietary strategies against epigenetic activation of COX-2 expression by AhR agonists.
- COX-2 is up-regulated by bradykinin in head and neck squamous cell carcinomas
- PGE2 greatly induced hepatocellular carcinoma cell adhesion, migration, and invasion by activating FAK/paxillin/Erk pathway.
- Manganese induces COX-2 by transcriptional up-regulation in human airway cells and the induction appears to be cooperatively mediated via multiple signaling pathways and GSH depletion.
- COX-2 overexpression is associated with worse survival among colon cancer patients. The effect of COX-2 on clinical outcome may be modified by p53 status.
- Cyclooxygenase-2-derived prostaglandin F2alpha mediates endothelium-dependent contractions in the renal artery with increased impact during aging.
- COX-2 overexpression represent important alterations that are related to the molecular pathways underpinning colorectal carcinogenesis
- Increased COX-2 expression in JPS patients was noted compared with patients with sporadic juvenile polyps (P < .001).
- Expression of COX-2 protein has no significant impact on the outcome of patients with colorectal cancer.
- Trends suggested down-modulation of cyclooxygenase-2 and Ki-67 in some tissues, increased pAKT-Ser473 expression, and an inverse relationship between PGE(2) and BCL2 expression.
- Mycobacterium bovis BCG (M. bovis BCG) downregulates tumour necrosis factor-alpha (TNF-alpha)-induced COX-2 gene expression in alveolar epithelial cells by inhibiting the phosphorylations of Raf-1 and p38 kinases.
- cyclooxygenase-2 that constantly induced by inflammation, has proved to be involved in the development of bladder carcinoma.
- Bacterial products (e.g., LPS) triggers a positive feedback loop involving COX-2/PGE(2) in biliary carcinoma cells and this second phase of EGFR phosphorylation is implicated in cell invasion by LPS
- TNF-alpha induces the activation of COX-2 by the up-regulation of MMP-9 via PGE2 receptors in cholangiocarcinoma.
- prostaglandin E2 production in oral squamous cell carcinoma cell lines was cyclooxygenase 2-dependent