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Validated All-in-One™ qPCR Primer for CDH1(NM_004360.4) Search again
Product ID:
HQP117736
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
Arc-1, BCDS1, CD324, CDHE, ECAD, LCAM, UVO
Gene Description:
cadherin 1
Target Gene Accession:
NM_004360.4(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
This gene is a classical cadherin from the cadherin superfamily. The encoded protein is a calcium dependent cell-cell adhesion glycoprotein comprised of five extracellular cadherin repeats, a transmembrane region and a highly conserved cytoplasmic tail. Mutations in this gene are correlated with gastric, breast, colorectal, thyroid and ovarian cancer. Loss of function is thought to contribute to progression in cancer by increasing proliferation, invasion, and/or metastasis. The ectodomain of this protein mediates bacterial adhesion to mammalian cells and the cytoplasmic domain is required for internalization. Identified transcript variants arise from mutation at consensus splice sites. [provided by RefSeq].
Gene References into function
- cell adhesion
- Human RB and c-Myc activate expression of the murine E-cadherin gene in epithelial cells through interaction with transcription factor AP-2
- Products of the c-myc gene activate or repress the activity of the E-cadherin promoter
- Both expression of E-cadherin and its membranous localization are required for well-differentiated-type morphogenesis in gallbladder cancer cells.
- Mutations and polymorphisms in E-cadherin gene CDH1, such as S270A, may contribute to the onset of prostate cancer (PCA) and warrant further investigations in other populations.
- The E-cadherin gene was potentially inactivated in a significant number of synovial sarcomas.
- Loss of E-cadherin may result in the disruption of the function of the cell-cell adhesion complex, which may cause weak cell-cell adhesion and confer invasive properties on a tumor.
- Cadherin-mediated cell sorting not determined by binding or adhesion specificity
- restoration of E-cadherin dependent adhsion in human protate carcinoma cells by expression of receptor protein-tyrosine phosphatase, PTPmu
- E-cadherin might be used as additional cell markers of Schwann cell-derived tumors.
- distinct methylation pattern in bladder cancer with frequent methylation of RARbeta, DAPK, E-cadherin, and p16.
- D257A & D370A mutations result in abnormal protein localization, changes in the actin cytoskeleton, reduced homophilic cell adhesion, and altered cell morphology; tumor-associated D370A mutation, but not the D257A mutation, induced increased cell motilit
- biological function of Cys(9) within the first repeat (the E-cadherin-derived N-terminal repeat)
- These results demonstrate that integrin-dependent cell to extracellular matrix adhesion reinforces E-cadherin-dependent cell-cell adhesion in Caco-2 cells.
- E-cadherin play important roles in esophageal carcinogenesis.
- The SLUG zinc-finger protein represses E-cadherin in breast cancer.
- Lateral dimerization of the E-cadherin extracellular domain is necessary but not sufficient for adhesive activity
- results suggest that the inadequate trophoblastic invasion, induced by antiphospholipid antibodies, can be the result of decreased alpha1 integrin and VE-cadherin and increased alpha5 integrin and E-cadherin expression in the trophoblast
- characterization of DNA polymorphism in promoter regions
- mucoepidermoid carcinoma of the thyroid (MECT)displays consistent neoexpression of P-cadherin and major alterations in the expression of E-cadherin and the three catenins
- Tumor-associated mutations of E-cadherin enhanced random cell movement of transfected MDA-MB-435S mammary carcinoma cells as compared to wild-type (wt) E-cadherin-expressing cells.
- restoration of cell adhesion by overexpression of nectin in HSC-39 cells
- Differential expression in human brain tumors
- E-cadherin expression in dental epithelium followed an apical-coronal gradient that was opposite to that observed for N-cadherin.
- CAS/CSE 1 stimulates E-cadhrin-dependent cell polarity in HT-29 human colon epithelial cells.
- promoter methylation studied in 80 patients with head and neck squamous cell carcinoma (HNSCC)
- role in regulating expression of the leucocyte common antigen-related tyrosine phosphatase
- Recovery of cellular E-cadherin precedes replenishment of estrogen receptor and estrogen-dependent proliferation of breast cancer cells rescued from a death stimulus.
- aberrant methylation preferentially occurs in invasive ductal breast cancer associated with poor prognosis and is one of the mechanisms of expression silence in breast cancers
- Src-induced disruption of E-cadherin localization requires specific integrin signalling.
- Data suggest that E-cadherin-mediated signaling through PI3-kinase can regulate the invasive behavior of cells by modulating proteinase secretion.
- Defected E-cadherin expression might play a role in the development of malignant phenotype in NSCLC
- ZEB1 plays a role in repressing E-cadherin and MUC1 in epithelial cells [ZEB-1]
- oxidative stress induces tyrosine phosphorylation and cellular redistribution of occludin-ZO-1 and E-cadherin-beta-catenin complexes by a tyrosine-kinase-dependent mechanism
- Downregulation of E-cadherin in melanocytes and melanoma cells by endothelin-1
- Altered expression of E-cadherin in hepatocellular carcinoma
- CpG hypermethylation was an important mechanism of E-cadherin gene inactivation in bladder cancer and also that specific CpG sites consistently presented higher methylation levels than others.
- E-cadherin promoter is subject to epigenetic control in colorectal ulceration and plays a role in the progression from chronic inflammation to colorectal cancer.
- E-cadherin polymorphism in prostate neoplasms
- CDH1 c-160a promotor polymorphism is not associated with risk of stomach cancer.
- germline E-cadherin mutations responsible for the predisposition to diffuse gastric cancer (DGC) among the Japanese
- Restoration of E-cadherin/beta-catenin expression in pancreatic cancer cells inhibits growth by induction of apoptosis.
- dimerization of E-cadherin is important for its cell adhesive properties
- In vivo recruitment of RB and AP-2 proteins on the E-cadherin promoter in MCF7 cells
- investigates whether E-cadherin is a substrate for calpain and whether calpain-dependent proteolysis was associated with prostate cancer progression
- E-cadherin is hypermethylated and shows low expression in colon and rectal neoplasms
- results indicate that expression of E-cadherin in IST-1 trophoblast cells results in a contact-mediated inhibition of motility and invasion and suggest an important role for E-cadherin down-regulation in the intermediate trophoblast during implantation
- in vivo evidence in cancer cells of the differential association between CpG methylation, MBPs, and histone modification in the entire CpG island of the human E-cadherin (CDH1) gene
- Involvement of the adhesive ligand pair CD103-E-cadherin in human thymocyte cell proliferation
- These data reveal a cooperative interaction between p120 catenin and E-cadherin and a novel role for p120 that is likely indispensable in normal cells.
- association of CDH1 haplotypes with susceptibility to sporadic diffuse gastric cancer
- clinical significance of E-cadherin and proliferating cell nuclear antigen expression in adenoid cystic carcinoma
- The reduction of E-cadherin and beta-catenin expression was related to invasiveness and proliferative status of prolactinomas and correlated with the more aggressive behavior of prolactinomas in men compared with in women.
- role in negative regulation of CD44-hyaluronan interaction
- promotion of E-cadherin and suppression of beta-catenin/T cell factor may be an important mechanism underlying the chemopreventive action of Ca(2+) in colon cancer
- Loss of E-cadherin expression followed by expression of the mts1 gene may be an important event for increasing cell proliferation, motility and invasion activity in the progression of gallbladder cancer.
- The presence of E-cadherin mutations can significantly alter the accumulation of the apoptosis-regulating p53 protein, whereas no correlation with the p53 mutation status or with Ki-67 staining was observed.
- Expression of e-cadherin and beta-catenin in human esophageal squamous cell carcinoma: relationships with prognosis.
- Abnormal E-cadherin and alpha-catenin and beta-catenin in pancreatic carcinoma tissues. Abnormal E-cadherin and alpha-catenin with differentiation, lymph node and liver metastases. Aberrant beta-catenin with lymph node and liver metastases.
- phosphorylation-dependent localization of CDH1 in vertebrate cells.
- CpG methylation and thus loss of E-cadherin is associated with metastasising laryngeal cancer.
- matrix metalloproteinase-2 and 9 and membrane-type 1 matrix metalloproteinase mRNA expression in endometriosis was higher than in normal endometrium whereas E-cadherin, alpha- and beta-catenin mRNA expression was not suppressed in endometriosis
- Pulse-labeled beta-catenin replaces the beta-catenin bound to the cell surface prebiotinylated E-cadherin immediately after synthesis or arrives at the plasma membrane in a complex with the E-cadherin precursor.
- Hypermethylation of an E-cadherin (CDH1) promoter region in high grade transitional cell carcinoma of the bladder comprising carcinoma in situ.
- study verified reduced expressions of adenomatous polyposis coli and E-cadherin proteins in colorectal cancer cells and suggests that normal protein expressions in benign epithelium are progressively and independently lost in sporadic colorectal cancers
- possibility that multiple pathways exist for E-cadherin entry into cells that are likely to reflect cell context and regulation.
- decreased expression of the E-cadherin catenin complex and methylation of the E-cadherin gene promoter region was found only in growth hormone cell adenomas with prominent fibrous bodies
- E-cadherin and claudins/occludin have roles in the regulation of tight junctions during the epithelium-mesenchyme transition, but are repressed by snail
- The molecular requirements for E-cadherin to activate Rac signaling thus appear distinct from those that stimulate PI3-kinase, and we postulate that p120-ctn may play a central role in the E-cadherin-Rac signaling pathway.
- Abnormal expression of E-cadherin was seen in mucoepidermoid carcinoma.
- High expression of E-cadherin is associated with the development of lymphatic tumor emboli
- dedifferentiation and a decreased expression of E-cadherin and ZO-1 are closely related to liver metastasis
- polymorphism of CDH-1 3'-UTR is a valid genetic marker for calcium stone disease.
- Findings identify E-cadherin as a novel substrate for matrilysin and indicate that shedding of E-cadherin ectodomain is required for epithelial repair.
- E-cadherin A/A genotype may be associated with susceptibility to urothelial cancer, but not with the progression of disease.
- The loss of E-cadherin rather than beta-catenin mutation is the crucial event in determining the differentiation 'level' of thyroid carcinomas
- Findings document the differential expression, subcellular localization and cell-cycle-regulatory activity of alternatively spliced human CDH1 isoforms.
- CDH1 inactivation due to mutations, LOH and methylation is associated with invasive and in situ lobular breast cancer.
- E-cadherin inhibits human mammary and prostate tumor cell invasion. The invasion suppressor signal is mediated through the beta-catenin-binding domain of the E-cadherin cytoplasmic tail.
- Methyl-CpG-binding protein 2 and promoter methylation cooperatively regulate E-cadherin gene expression in colorectal carcinoma
- Single nucleotide polymorphism in the E-cadherin gene promoter is associated with tumorigenesis and progression of gastric carcinoma
- Expression of HPV16 E6 in keratinocyes decreases expression of cell surface E-cadherin thereby depleting langerhans cells at the site of infection
- Data demonstrate a direct role of E-cadherin/catenin complex organization in the regulation of matrix metalloproteinases and suggest an implication of this regulation in the expression of an invasive phenotype by bronchial tumor cells.
- Bcl-2 expression decreases the level of functional E-cadherin thereby interfering with junction formation
- Results suggested that human embryos and blastocysts could express E-cadherin and the expression increased during their development.
- the -160 C/A polymorphism of E-cadherin is not directly involved in Korean gastric cancer development
- provides support that E-cadherin induction by WNT/beta-catenin signaling is an evolutionarily conserved pathway operative in lung cancer cells and that loss of expression may be important in lung cancer development or progression
- E-cadherin has a role in tumorigenicity and metastasis
- Hypoxia induces down-regulation of E-cadherin in ovarian carcinoma cells, via up-regulation of the transcriptional repressor SNAIL.
- E-cadherin-mediated cell adhesion and apoptosis of prostatic cancer cells are regulated by ligand activation of the androgen receptor
- E-cadherin affected the regulation of cell proliferation, differentiation and adhesion, and decreased chemosensitivity
- the comparable region of N-cadherin can substitute for this required region in E-cadherin and is required for suppression by the mutant form of N-cadherin that is capable of suppressing
- The frequencies of E-cadherin promoter hypermethylation appear to be correlated with more advanced stage of squamous carcinogenesis in skin.
- A recombinant E-cadherin lacking free sulfhydryl groups and its mutants with novel cysteines were expressed. The coexistence of the structurally identical adhesive and lateral dimers suggests some flexibility of the extracellular cadherin region.
- Pancreatic cancer likely occurs in case of the inactivation of E-cadherin and alpha-catenin genes and abnormal expression of proteins
- We conclude, therefore, that two major components of cell-cell interaction synergistically regulate cell cycle progression in HEK293 cells by regulating p21 expression in a beta-catenin/TCF-dependent manner.
- Intragenic deletion of CDH1 is the activating mechanism of the wild-type allele in hereditary diffuse gastric carcinoma.
- In human melanocytic tumors, a causative role of (loss of ) E-cadherin or (gain of ) N-cadherin for melanocytic tumor progression still remains to be proven.
- E-cadherin and epidermal growth factor receptor (EGFR) are associated in mammary epithelial cells and that E-cadherin engagement in these cells induces transient activation of EGFR, as previously seen in keratinocytes.
- an 80 kDa fragment of E-cadherin has a role in the metastatic progression of prostate cancer
- E-cadherin mediated adhesion and signaling in mammalian epithelial cells requires homolog of disc-large
- investigation of whether the -347G-->GA single nucleotide polymorphism affects the transcriptional activity of the E-cadherin gene
- Low expression of E-cadherin is associated with late cervical metastasis in stage I and II invasive squamous cell carcinoma of the oral tongue
- FAM associates with E-cadherin and beta-catenin during trafficking to the plasma membrane
- Aberrant methylation of CDH1 is associated with recurrent cervical cancer
- Promoter hypermethylation of E-cadherin and its abnormal expression in Epstein-Barr virus-associated gastric carcinoma
- endogenous PGE2 is involved in the hBD-2 and E-cadherin responses of human gingival epithelial cells to A. actinomycetemcomitans. HGEC exposed to A. actinomycetemcomitans showed a decrease in E-cadherin levels.
- EphA2 and E-cadherin may play an important role in tumor metastasis in colorectal cancer
- single nucleotide polymorphism in CDH1 is a low-penetrant prostate cancer susceptibility gene
- Cdx1 or Cdx2 expression is sufficient to induce E-cadherin-dependent adhesion of COLO 205 cells associated with polarization and cell-cell membrane compaction, as well as induction of differentiated gene-expression pattern.
- Combined evaluation of VEGF and E-cadherin levels may become a useful indicator of NSCLC biological behavior and provide clinically important evidence on which to base treatment in NSCLC.
- E-cadherin plays an important role in regulating the invasive potential of prostate cancer cells through an unique paracrine mechanism.
- promoter hypermethylation and consequent downregulated of E-cadherin is significantly associated with gastric carcinomas of the diffuse histotype
- Results identify a necessary role for cortactin in the cadherin-actin cooperation that supports productive contact formation.
- E-cadherin-mediated adhesion mechanisms have a role in sperm-oolemma interactions
- Snail is involved in both the direct transcriptional repression of genes, such as E-cadherin and occludin, and post-transcriptional events, including downregulation of claudin-1
- SH2 and SH3 domains of Src mediate peripheral accumulation of phospho-myosin, leading to integrin adhesion complex assembly, whereas loss of SH2 or SH3 function restores normal regulation of E-cadherin and inhibits vimentin expression
- CDH1 methylation and E-cadherin expression are related and have a role in progression of diffuse gastric cancer
- E-cadherin has a role in preventing peritoneal dissemination in gastric cancer
- The absence of dermal invasion of nevus cells could be due to the expression of E-cadherin in these cells in reconstructed epidermis.
- E- to N-cadherin switching in epithelial carcinomas has a potential impact on metastatic progression.
- Cytoplasmic p120ctn may contribute to the invasive phenotype of E-cadherin-deficient breast cancer cells.
- determination of CDH1 promoter methylation in breast tumors with decreased or absent E-cadherin protein expression
- E-cadherin-mediated cell adhesion is required for keratinocyte-mediated control of melanocytic cells, which can override proliferative activity of beta-catenin.
- E-cadherin -347 G-->GA polymorphism may be associated with colorectal cancer.
- Thirteen novel CDH1 mutations found in diffuse gastric cancer families.
- Hypermethylation of CDH1 is statistically significantly associated with poor outcome in cervical cancer.
- the establishment of E-cadherin-based cell-cell adhesion requires Rap1
- E-cadherin and p16INK4a are commonly methylated in non-small cell lung cancer
- mutant E-cadherin significantly alters the dynamics of cell adhesion and motility in living cells
- Data showed that intestinal metaplasia is associated with E-cadherin down-regulation in gastric mucosa, whereas H. pylori infection does not seem to play a direct role in this process.
- E-cadherin and calretinin are sensitive and specific in differential diagnosis of benign and malignant serous effusion specimens.
- abnormal immunhistochemical E-cadherin and beta-catenin expression is associated with changes in pit pattern in invasive colorectal neoplasms
- Review summarizes divergent studies that provide evidence of the function of E-cadherin trafficking and the puzzle of how this adhesion molecule is regulated and managed throughout the life of the epithelial cell.
- E-cadherin mutations have no influence on expression of genes involved in Wnt-signaling, but they may promote their own expression by blocking upregulation of E-cadherin repressors.
- Most invasive and metastatic areas of oral squamous cell carcinoma showed reduced expression and methylation of E-cadherin.
- Decreased E-cadherin expression is an independent prognostic factor for disease progression and mortality in pathological stage I-III endometrial cancer.
- T lymphocyte development can proceed independently of alphaEbeta7/E-cadherin interactions
- Results point to a functional link between matrix metalloproteinase-3 and E-cadherin
- role in tumor genesis and progress of hereditary gastric carcinoma
- E-cadherin downregulation is associated with the loss or absence of glandular epithelial differentiation in certain synovial sarcoma
- The E-Cadherin, the main system of adherens junction, present in the tight junctions in HepG2 cells.
- conjoint endocytosis and trafficking is a novel mechanism for the coregulation of E-cadherin and FGFR1 during cell signaling and morphogenesis
- the interaction of Pnn with the corepressor CtBP1 may modulate repression of E-cadherin transcription by CtBP1
- CDHE expression is repressed in the lower crypt of small intestine and is a biological marker of functional relevance.
- E-cadherin-deficiency in metastatic cancer may in some cases be due to p120 downregulation [review]
- E-cadherin may have a role in progression of squamous cell carcinoma
- heregulin stimulates aggregation and inhibits invasion of MCF-7/6 cells via activation of the E-cadherin/catenin complex
- E-cadherin gene C-160A promoter polymorphism may not play a major role in the etiology of non-cardia gastric cancer in Chinese population.
- Change in the location of E-cadherin expression (from membrane cytoplasm) is strongly associated with an increased aggressiveness of colrectal cancer.
- Wnt signaling stabilizes Snail and beta-catenin proteins in tandem fashion so as to cooperatively engage transcriptional programs that control an epithelial-mesenchymal transition.
- Loss of expression of E-cadherin and beta-catenin may play an important role in the progression of pulmonary adenocarcinoma
- Aberrant E-cadherin is result of point mutation in exon 9 donor splice site causing skipping of exon 9 with consequent deletion of corresponding amino acids. Leads to disturbed cell adhesion. Mediates formation of cadherin/ catenin complex.
- These results provide a new example of Rho GTPase regulation of basolateral trafficking and demonstrate novel roles for Cdc42 and Rac1 in the post-Golgi transport of E-cadherin.
- a novel pathway for Rab11 dependent, dileucine-mediated, mu1B-independent sorting and basolateral trafficking, exemplified by E-cadherin
- Data suggest when carcinoma in a gastric biopsy is negative for E-cadherin staining, metastatic breast carcinoma should be considered.
- Altered E-cadherin adhesion complex is an early event affecting atypical lobular hyperplasia as well as lobular carcinoma in situ and occurs prior to progression to invasive disease.
- All 61 meningothelial meningiomas, 10 of 12 invasive meningiomas, and 3 of 5 anaplastic meningiomas were positive for both ECAD and beta-catenin, while these were both negative in all of the fibrous meningiomas.
- Tumors with reduced E-cadherin expression invaded deeper, had more lymph node metastasis, and had more lymphatic invasion than the tumors with preserved E-cadherin expression.
- cadherin switching (downregulation of E-cadherin and upregulation of N-cadherin) is necessary for increased motility but is not required for the morphological changes that accompany the epithelium-to-mesenchyme transition
- Disruption of E-cadherin-mediated cell-cell contacts at high cell density inhibits the induction of p27(kip1) and restores proliferation in contact-inhibited cells.
- association between decreased expression and metastatic Wilms' tumor
- dysfunction of E-cadherin and nm23 has a role in progression of NSCLC
- mutations cause inactivation of the cell adhesion protein E-cadherin; carriers of the CDH1 germline gene mutation develop an aggressive, diffuse, submucosal gastric cancer at an early age [review]
- E-cadherin expression was significantly associated with higher tumour grade in colorectal carcinoma.
- These findings suggest that alteration of the E-cadherin pathway can contribute to human clefting.
- examined here the effect of trans-interacting nectin on non-trans-interacting E-cadherin endocytosis
- E-cadherin may play a distinct role in the development of ovarian epithelial cancers.
- Strong E-cadherin expression in lymph node metastases was highly predictive of improved survival.
- The entire cadherin-catenin complex is involved when assessing its prognostic value in colonic adenocarcinom.
- disturbances in the distribution of beta-catenin and E-cadherin might affect the morphology of adenoid cystic carcinoma
- ADAM10 has a role in E-cadherin shedding and epithelial cell-cell adhesion, migration, and beta-catenin translocation
- Domain 5 of E-cadherin may play a critical role in the regulation of heterophilic adhesion to integrin alphaEbeta7; domains 1, 2, 3, and 4 are involved in homophilic adhesion.
- expression at transcriptional level is repressed by HBV X protein
- SIP1 sumoylation by Pc2 attenuates transcriptional repression of E-cadherin
- an E-cadherin germline mutation may have a role in development of hereditary diffuse gastric cancer
- E-cadherin distribution in human embryos is stage-dependent
- Patients with the -160C/C genotype might require H. pylori infection to promote inactivation of CDH1, suggesting that H. pylori infection might affect gastric carcinomas in initial stage because polymorphism is germ line.
- Reduced E-cadherin is a common genetic phenotype of gastric cancers and plays beneficial roles in tumor metastasis.
- upon infection of quiescent cells human cytomegalovirus not only activates the E2F-dependent G(1)/S transcription program but also facilitates protein accumulation of APC/C substrates by rapid Cdh1 dissociation
- E-cadherin may have a role in progression and recurrence of transitional cell carcinomas of the urinary bladder
- The E-cadherin is a cell-cell adhesion protein expressed in cytotrophoblasts, which is lost as they differentiate and syncytialise.
- loss of E-cadherin-mediated adhesion plays a causal role in the transition from low- to high-grade squamous cell carcinoma
- E-cadherin protein was lost and mRNA levels were significantly decreased in prostate cancer cells expressing kallikrein 4 and prostate specific antigen.
- report strong confirmation of the association between prostate cancer risk in FH+ cases and a functional CDH1 promoter SNP in an independent population
- inhibition of E-cadherin-dependent cell-cell adhesion led to the genetic reprogramming of tumor cells
- -160(C-->A) polymorphism in CDH1 gene promoter region may not be in association with genetic susceptibility to gastric cancer in Chinese population from Fujian.
- The TGFbeta(1)-induced destabilisation of E-cadherin-mediated cell-cell adhesion involves phosphorylation of beta-catenin, which is regulated by E-cadherin adhesion complex-associated PI3-kinase and PTEN.
- Increased expression of delta-catenin os associated with the down-regulation and redistibution of ECAD and p120ctn in prostatic cancer.
- Cell-to-cell communication mediated by E-cadherin contributes to the acquirement of a cardiomyogenic phenotype of human endothelial progenitor cells.
- With tumor progression and development of heterogeneity, the abnormal expressions of MMP-9, TIMP-2, and E-cadherin or DNA aneuploid rate or high SPF gradually increases, suggesting that they play a crucial role in gastric carcinoma progression
- Depressed E-cadherin correlates with HBxAg trans-activation function.
- CDH-1 is closely related to metalloproteinase and plays important but not well-understood role in onset and progression of primary open angle glaucoma. Role could be resolved by posttranslated products of gene and protein-protein interaction.
- expression of E-cadherin and beta-catenin is significantly down regulated in prostate cancer compared to surrounding benign appearing prostate, which correlates with increasing Gleason grade
- The CDH-1 gene 3'-UTR C/T polymorphism is associated with prostate cancer. The 'CC' homozygote indicates a relatively higher risk for developing prostate cancer than other genotypes.
- In testicular tumours, as in other neoplasms, dysadherin downregulates E-cadherin expression, at least in part
- E-cadherin controls enterocyte-specific expression of genes, such as the apoA-IV gene, through the control of hepatic nuclear factor 4alpha nuclear abundance
- These results suggest that Scrib stabilizes the coupling between E-cadherin and the catenins and are consistent with the idea that mammalian Scrib could behave as a tumor suppressor by regulating epithelial cell adhesion and migration.
- transforming growth factor-beta1 overexpression and alteration in E-cadherin/beta-catenin complexes in bladder urothelium might play a crucial role in urinary bladder carcinogenesis in humans exposed to long-term low-dose ionizing radiation
- Data indicate that E-cadherin may modulate Wnt-dependent gene expression in DLD-1 colorectal cancer cells by regulating the availability of beta-catenin.
- CDH1 may be a low-penetrant prostate cancer susceptibility gene.
- Increase in HOXA1 expression in mammary carcinoma cells at full confluence is E-cadherin-dependent.
- Results suggest that loss of E-cadherin function is linked to regulation of cell-cell and cell-matrix adhesion, based in part on cell surface expression of alpha2, alpha3 and beta1 integrins.
- decreased immunoreactivity of E-cadherin in esophageal squamous cell carcinoma was statistically correlated with presence of lymphatic metastases
- Our present results show that gastric differentiated-type carcinomas have different characteristics according to the phenotypic marker expression of the tumour in terms of histological findings, E-cadherin expression and pattern of chromosomal changes.
- Data suggest that tissue expression of E-cadherin could be a useful marker to predict the progression and metastasis of hepatocellular carcinoma.
- CDH1 promoter methylation, but not mutational inactivation, is part of an entire programme, resulting in epithelial-mesenchymal transition and increased invasiveness in breast cancer
- PCP-2 may play an important role in the maintenance of epithelial integrity, and a loss of its regulatory function may be an alternative mechanism for activating beta-catenin signaling.
- Loss of E-cadherin and Death Associated Protein kinase methylation and expression is more frequent in lymph node metastases of pancreatic adenocarcinoma
- Data show that dynamic microtubules regulate the local concentration of E-cadherin at cell-cell contacts.
- Serum levels may be a prognostic biological marker innonsmall cell lung cancer.
- Findings demonstrate a stimulatory role for E-cadherin in proliferative regulation, and identify a simple mechanism by which cell-cell contact may trigger or inhibit epithelial cell proliferation in different settings.
- Reduced E-cadherin expression is related to a poor prognosis through hematogenous metastasis in pulmonary adenocarcinoma.
- The high frequency of methylation of the CDH1 gene promoter suggests that the inactivation of tumor suppressor genes and of the genes related to the control of cellular proliferation through this mechanism is involved in gallbladder carcinogenesis.
- E-cadherin pathway is a novel and functionally important mediator by which changes in Kruppel-like KLF6 tumor suppressor can directly alter ovarian tumor invasion and metastasis.
- Activation of protease-activated receptor-2 (PAR2) interrupted adhesion of E-cadherin-expressing L cells and of primary airway epithelial cells to immobilized E-cadherin extracellular domain. Activation of PAR2 interrupts E-cadherin adhesion.
- These data suggest that endocytosis is the main pathway for the dissociation of E-cadherin adhesive dimers.
- E-cadherin has a role in head and neck squamous cell carcinoma [review]
- the degradation of E-cadherin in response to expression of R-cadherin is due to competition for p120(ctn)
- No significant association between E-cadherin expression and tumor grade, stage, age or gender of the patients, the number of recurrences, or overall survival could be seen.
- CDH1 mutations are associated with a risk of early-onset gastric cancer.
- Levels of expression of CtBP and p300 are critical for the action of SNAIL and ZEB1, which have a pivotal role in levels of epithelial-mesenchymsal transitionin human colon carcinoma.
- E-cadherin immunoreactivity was detected in all the epithelial tissues examined, except adrenal cortical cells and granulosa cells.
- The mechanism underlying 5-Azacytidine's anti-metastasis activity is associated with restored functional expression of E-cadherin in ovarian cancer.
- E-cadherin/CDH1 gene methylation is an important cause for its gene silence in diffuse variant gastric carcinoma.
- Examination of E-cadherin expression and distribution in colorectal tumors can be extremely valuable in predicting disease recurrence.
- A novel mutation in the E-cadherin gene in a family with hereditary diffuse gastric cancer. The presence of a 1610delC germline mutation was confirmed.
- CDH1 serum levels may be a serological marker for staging of patients with testicular germ cell neoplasia.
- Our results indicate a functional role of Met-E-cadherin interaction in MCF-7 cells through the amplification of the signaling downstream of HGF-Met triggering that involved c-Src and phosphoinositide-3-kinase activities.
- A model is proposed to infer the pathogenic significance of CDH1 germline missense variants.
- CD24 regulates E-cadherin and TGF-beta3 expression in cultured oral epithelial cells
- dysfunction of E-cadherin due to its endocytosis may occur in some proportion of human breast carcinomas in which the PP2A-A protein is lost or significantly reduced
- the gain and not the loss of the E-cadherin axis contributes to the invasiveness of inflammatory breast cancer cells unique phenotype
- Roles of E-cadherin and beta-catenin complexes in signet ring cell carcinoma of the lung differ from their roles in gastric or colorectal cancers.
- loss of extracellular E-cadherin observed in normal duodenal & colonic mucosa in patients familial adenomatous polyposis might play a role in high susceptibility of these tissues for (pre-) malignant transformation
- E-cadherin may sensitize human melanoma cells towards apoptosis
- E-cadherin expression responds only to the combination treatment and not to single PPARgamma agonists, defining a new class of PPARgamma target genes
- SCCA2 regulates cell migration and invasion via E-cadherin expression, suggesting that SCCA2 may be involved in cancer behavior such as invasion or metastasis.
- Increased N-cadherin expression was found in pseudomyxoma peritonei.
- SMAD family member 1 is involved in the progression of pancreatic cancer and plays a role in mediating signal transduction from collagen type I to downregulate E-cadherin expression.
- In conclusion, ROS play a central role in mediating TPA-triggered sustained PKC and ERK signaling for regulation of gene expression of integrins and E-cahedrin that are responsible for EMT and migration of HepG2.
- VHL promotes E2 box-dependent E-cadherin transcription by HIF-mediated regulation of SIP1 and snail
- Real-time reverse transcription-PCR and Western blotting were used to assess levels of E-cadherin expression in esophageal cancer.
- first CDH1 germline mutation of an Italian family with hereditary diffuse gastric cancer is reported
- Cell cycle regulation of Six1 occurs both transcriptionally and post-translationally via phosphorylation
- E-cadherin repression is necessary for c-Myc-induced cell transformation.
- alpha2-antiplasmin induction inhibits E-cadherin processing mediated by the plasminogen activator/plasmin system, leading to suppression of progression of oral squamous cell carcinoma via upregulation of cell-cell adhesion
- Found in in situ lesions. May play some role in the prognosis/invasion of extramammary Paget's disease.
- Seven novel mutations within the CDH1 gene are associated with Hereditary diffuse gastric cancer.
- targeting constitutive expression of AP-2alpha in AP-2-positive KM12C colon cancer cells with small interfering RNA resulted in an increase in their invasive potential, downregulation of E-cadherin and increased expression of MMP-9
- These results indicate that perturbation of the E-cadherin/beta-catenin complex by H. pylori CagA plays an important role in the development of intestinal metaplasia.
- the recruitment of PI3K to the E-cadherin/beta-catenin/p120-catenin complex via beta-catenin at the plasma membrane is required for calcium-induced phospholipase C-gamma1 activation and, ultimately, keratinocyte differentiation
- PIPKIgamma links E-cadherin to adaptor protein complexes
- E-cad expression to be correlated with E-cad methylation at highly statistically significant levels. Above a threshold of approximately 20% to 30% mean methylation, the expression of E-cad was effectively silenced.
- High Nonmembranous type E-cadherin expression correlated significantly with lymph node metastasis, distant metastasis, and recurrence regulated by hepatocyte growth factor
- Cadherin-E interaction with integrin alphaEbeta7 causes antitumor cytotoxic response by CD8+/CD103+ tumor-reactive T lymphocytes.
- C. albicans invades mucosal tissues by promoting the proteolytic degradation of E-cadherin in epithelial adherens junctions, mediated by transcription factor Rim101 and Sap5 proteins.
- Decreased E-cadherin expression is associated with advanced gallbladder cancers
- CDHE was expressed in both tumor types, especially in the cytoplasm and cell membrane of the cuboidal cells and to a lesser extent in the polygonal cell membrane, where it was expressed mostly in the cytoplasm.
- E-cadherin cleavage is enhanced by contact with C. albicans: intracellular cleavage generating substrate for gamma-secretase and extracellular cleavage temporally associated with increase in monolayer permeability.
- Data show tha E-cadherin homophilic binding independent of other cell contacts directly transduces growth inhibition by a beta-catenin-dependent mechanism that inhibits selective signaling functions of growth factor receptors.
- incubation with HGF mediated the release of MMP-7, resulting in extracellular cleavage of E-cadherin from stomach cancer cells
- Data show that E-cadherin/beta-catenin-based adherens junctions are dispensable for tight junction formation and apical lumen biogenesis but not for apical lumen remodeling.
- Decreased E-cadherin is asociated with thyroid cancer
- E-cadherin promoter hypermethylation was observed in the tumour of the P373L mutation carrier.
- None of the 30 infiltrating lobular carcinomas cells showed preserved E-cadherin expression.
- Together, these findings demonstrate a role for SNX1 in retrieval of E-cadherin from a degradative endosomal pathway and in membrane trafficking pathways that regulate E-cadherin recycling.
- Differentially regulated beta-catenin pools associate with the E-cadherin-gamma-secretase adherens junction complex; one pool regulated by gamma-secretase is important to intestinal epithelial cell homeostasis.
- Characterization of endogenous CDHE-CTNNB complexes with ELISA represents a dramatic improvement over other assays.
- While CDH1 methylation seems to be an early event in Hp gastritis, MLH1 methylation occurs late along with IM.
- E-cad promoter methylation may play a role in tumor cell differentiation and perineural invasion.
- Recurrent CDH1 mutations in families with hereditary diffuse gastric cancer are due to both independent mutational events and common ancestry. The presence of a founder mutation from Newfoundland is strongly supported.
- results of this study show no association exists between the E-cadherin genotype and the risk of tumor recurrence in Chinese patients with hepatocellular carcinoma
- Downregulation of E-cadhedrin expression is associataed with increased EGFR downstream signalling and a subsequent increase in expression of Th2-attracting chemokine TARC.
- The C/A polymorphism of CDHE has a direct effect on the risk of diffuse gastric cancer at young age in Mexican population.
- E-cadherin signaling is an important activator of c-Src at cell-cell contacts, providing a key input into a signaling pathway where quantitative changes in signal strength may result in qualitative differences in functional outcome.
- we explored the implication of three proteins (E-cadherin, a- and b-catenins) that form the cadherin-catenin complex, a receptorial structure strictly involved in tumoral vascular invasion and embolization in this biologic event
- Aberrant E-cadherin expressions were described in several tumors such as in bladder cancer. This was also found to be correlated with tumor invasion and survival.
- A tight control of E-cadherin expression depending on the differentiation stage of the progenitor cells, is suggested.
- In addition to suppressing late-stage tumor progression, E-cadherin-mediated adherens junctions may also contribute to the initial emergence of a cohesive morphogenic phenotype that is a hallmark of differentiated epithelial ovarian carcinoma.
- NFkappaB activation mediated by loss of E-cadherin may represent an essential, even initial event in colorectal neoplasm metastasis
- study demonstrates that E-cadherin represents a ligand for KLRG1 and that ligation of KLRG1 by E-cadherin inhibited effector cell functions of polyclonal NK cells
- E-cadherin thus requires both ankyrin-G and beta-2-spectrin for its cellular localization in early embryos as well as cultured epithelial cells.
- Junctional adhesion molecule-A is critical for the formation of pseudocanaliculi and modulates E-cadherin expression in hepatic cells
- Results show E-cadherin-mediated Listeria internalization requires Arp2/3 complex acts as an actin nucleator.
- 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.
- Ep-CAM cross signaling with N-cadherin involves Pi3K, resulting in the abrogation of the cadherin adhesion complexes in epithelial cells.
- High level E-cadherin expression and p120ctn localization were associated with esophageal squamous cell carcinoma differentiation and lymph node metastasis
- there are significant differences of expression of E-cadherin between primary breast cancer cells and their metastases
- Aberrant methylation of multiple genes (E-cadherin, estrogen receptor, RB1 , p16, p15, p14, and MGMT) is involved in gastric carcinogenesis.
- presence of the A allele of the -160C/A polymorphism in the E-cadherin gene may be a risk factor for prostate cancer in the Japanese population
- a relation between the E-cadherin 3'-UTR C --> T polymorphism, the -160 A/-347 GA haplotype of two promoter polymorphisms and risk of endometriosis
- A novel germline CDH1 truncating mutation in the extracellular portion of the protein (517insA) was found in 2 relatives with lobular breast cancer. Germline CDH1 mutations can be associated with invasive LBC in the absence of diffuse gastric cancer.
- E-cadherin and beta-catenin have roles in progression of Epstein-Barr virus-associated gastric carcinoma
- The previously reported characteristics of this mutation, E-cadherin (V832M) do not apply to human epithelial cells expressing this mutant protein.
- Expression may be reduced in some early gastric carcinomas.
- The E-cadherin gene methylation presence in tumors with lowest invasive and metastatic potential suggests the early involvement of this epigenetic event in the multistep progression of the oral carcinogenesis
- E-cadherin immunostaining was less intense in metaplastic cervical epithelial cells of women on tibolone, whereas hormone therapy and raloxifene were not associated with altered E-cadherin expression.
- These results demonstrate that lysophosphatidic acid regulates c-Met function through PKC delta and E-cadherin.
- E-cad expression in gastric carcinoma is relatively low in the internal obstruction of stagnant toxin type and the in-coordination between liver and stomach type.
- Analysis of interface of In1a protein with E-cadherin to identify single amino acid substitutions in InlA that would potentially improve the overall quality of interaction and hence increase the weak binding affinity of the complex
- These data suggest that serine/threonine phosphorylation of p120 influences the dynamics of E-cadherin in junctions.
- Our findings suggest that the hypermethylation of E-cadherin promoter might be involved in the process of gastric carcinoma through the specialized factors in H. pylori-induced enlarged fold gastritis.
- convincing evidence that cadherin adhesion is based on high-affinity cadherin-cadherin interactions
- MUC1 may affect cancer cell migration by increasing E-cadherin/beta-catenin complex formation and restoring E-cadherin membrane localization
- Re-expression of E-cadherin in HT29(US) cells restored the ability of caveolin-1 to down-regulate beta-catenin-Tcf/Lef-dependent transcription and survivin expression, as seen in HT29(ATCC) cells.
- Our results suggest that methylation of E-cadherin is a frequent, early event in gastric carcinoma progression. Two factors were ...associated with lymph node metastasis: abnormal expression of E-cadherin and lymphatic invasion
- Kallikrein 6 induces E-cadherin shedding and promotes cell proliferation, migration, and invasion.
- Reduced expression of E-cadherin was associated with short overall survival incolorectal neoplasms
- Altogether, our results suggested that E-cadherin mediated cell-cell adhesion was essential for preventing the proteasome degradation of PTEN/
- Comparison of the E-cadherin structure with other type I cadherin structures reveals features that are likely to be critical to facilitate dimerization by strand exchange as well as dimer flexibility.
- ATCTG and CTTTG CDH1 haplotypes may be associated with an increased risk and decreased risk, respectively, of gastric cancer in Japan.
- tumor-specific downregulation of expression and methylation of CDH13 and CDH1, alone or in combination, may be involved in the development and invasive growth of pituitary adenomas.
- This paper focuses on changes in E-cadherin (CDH1), adenomatous polyposis coli (APC), and beta-catenin (CTNNB1) in 50 tumors of the central nervous system
- there is an aberrant nuclear localization of E-cadherin in CC-RCC harboring VHL mutations, suggesting potential prognostic value of VHL and E-cadherin in CC-RCC.
- findings suggest E-cadherin-dependent cell-cell contact, directly or indirectly, mediates signal to undergo apoptosis of CaSki cells during multicellular tumor spheroid formation & provides new information on role of E-cadherin in cervix cancer apoptosis
- Data suggest that Dia1 localizes to and controls E-cadherin-mediated junctions in a RhoA-dependent manner.
- Somatic E-cadherin mutations affect apoptosis regulation in that way that they can facilitate the disruption of adherens junctions thereby possibly influencing the response to cisplatin-based chemotherapy.
- Report a potential association of variants in the CCND1 and CDH1 genes with familial colorectal cancer using a unique study design with phenotypic extremes.
- The current findings suggested that simultaneous methylation of the E-cadherin and H-cadherin genes occurs in a subset of NSCLCs
- -160A of the E-cadherin gene is emerging as a low-penetrance tumor susceptibility allele for the development of gastric, lung, prostate, and urothelial cancers.
- functional significance of combined dysregulation of PKD1 and E-cadherin in prostate cancer; their effect on cell growth is mediated by beta-catenin.
- removal of N-glycans on E-cadherin resulted in elevated tyrosine phosphorylation level of beta-catenin and reduced beta- and alpha-catenins at adherens junctions
- genetic predisposition plays role in hereditary diffuse gastric cancer
- analysis of Epstein-Barr virus, beta-catenin, and E-cadherin in gastric carcinomas
- Therefore, a loss of cell-cell junctions, a key process that occurs during the epithelial-mesenchymal transition, should have a broad impact on ER alpha transcriptional functions.
- KCC3 down-regulates E-cadherin/beta-catenin complex formation by inhibiting transcription of E-cadherin gene and accelerating proteosome-dependent degradation of beta-catenin protein
- membranous overexpression of E-cadherin and beta-catenin are associated with the metastatic prostate cancer cells in bone and the high frequency of expression suggests their involvement in the intercellular adhesion of the metastatic cells in bone
- The C/C genotype of 3'-UTR C/T SNP and -160C/-374GA haplotype in E-cadherin gene may be a factor for risk of epithelial ovarian cancer in Chinese; the lower expression of E-cadherin might play a role in the pathogenesis of epithelial ovarian cancer.
- A high frequency of hypermethylation was detected in CDH1 and SFN genes in tumoral and normal cortex tissues.
- In most hereditary cancer syndromes, like hereditory diffuse gastric cancer and lobular carcinoma of the breast, multiple organ sites are affected by cancer and have been shown to be associated with germline mutations in CDH1 at 16q22.1.
- Silencing Cdc42 blocks activation of EGFR and Src induced by Ca2+ depletion, resulting in a reduction in E-cadherin degradation
- Using transient promoter assays, we show that Twist can down-regulate E-cadherin promoter activity by up to two folds.
- the CaR regulates cell survival and Ca(2+)(o)-induced differentiation in keratinocytes at least in part by activating the E-cadherin/PI3K pathway through a Src family tyrosine kinase-mediated signaling
- in addition to the previously implicated tumor suppressor activity of E-cadherin, modified forms of this glycoprotein might also play a role in growth promotion
- Micrometastasis was significantly correlated with the depth of invasion, tumor size, operation method, Lauren classification, lymphovascular invasion and loss of E-cadherin expression in primary tumor.
- that the heterogeneous pattern of SCCA and E-cadherin in primary lesions is strongly associated with the high incidence of lymph node metastasis in cervical squamous cell carcinoma
- changes of Ecadherin (CDH1) and beta-catenin (CTNNB1) genes in two central nervous system germ cell tumors are reported; both germ cell tumors analyzed demonstrated LOH of the CDH1 gene
- the APC has a novel role in UV-induced cell death; APC/CDH1 is regulated through proteolysis
- E-cadherin expression is frequently reduced in laryngeal squamous epithelium of patients with laryngopharyneal reflux.
- Rac signaling to cyclin D1 is a crucial pro-proliferative effect of E-cadherin-mediated cell-cell adhesion
- in solid pseudopapillary neoplasm of the pancreas E-cadherin expression moved from membranous to intracytoplasmic localization
- The CDH1 C-160A polymorphism is not associated with the risk of CRC in the German population
- The present study indicates that CDH1 single nucleotide polymorphisms might modify susceptibility to esophageal squamous cell carcinomas and gastric cardia adenocarcinomas
- ADAM10-mediated E-cadherin proteolysis leads to the impaired cohesion of keratinocytes observed in eczematous dermatitis.
- Noncohesive pancreatic cancers were characterized by the loss of E-cadherin protein expression. Promoter hypermethylation is a possible mechanism of E-cadherin gene silencing in a subset of these cancers.
- The E-cadherin-repressed hNanos1 gene induces tumor cell invasion by upregulating MT1-MMP expression.
- The expressions of aPKC-iota and E-cadherin may reflect the differentiation and invasive potential of cholangiocarcinoma
- E-cadherin mutant missing N-glycans at Asn554, Asn566 and Asn618 failed to induce cell cycle arrest in G1 phase and to suppress cell proliferation in comparison with wild-type E-cadherin.
- Increased histone acetylation might be responsible for PGC-1alpha-mediated transactivation of a minimal E-cadherin promoter.
- study describes activation of EGFR by mutant E-cadherin as a novel mechanism in tumor cells that explains the enhanced motility of tumor cells in the presence of an extracellular mutation of E-cadherin
- Vpu leads to the depression of both total and beta-catenin-associated E-cadherin levels through beta-TrCP-dependent stabilization of the transcriptional repressor Snail.
- PTPRK influences transactivating activity of beta-catenin in non-tumoral and neoplastic cells by regulating the balance between signaling and adhesive beta-catenin, thus providing biochemical basis for the hypothesis of PTPRK as a tumor suppressor gene.
- Decreased E-cadherin may be important in the development of endometrial endometrioid carcinoma.
- Combined analysis of Cripto-1 and E-cadherin has significant value in evaluating the metastatic potential of gastric cancer and predicting patient prognosis.
- levels in colon carcinomas were not statistically different from levels in adjacent normal mucosa and were not correlated with tumor, nodes, and metastases stage
- The disassembly of E-cadherin complexes from junctions in human keratinocytes was induced by Rac1 and Rac3 via activation of the Rac target PAK1.
- These results lead to a new hypothesis that Snail and ZEB1 are downstream of CCN6 and play a critical role in CCN6-mediated regulation of E-cadherin in breast cancer.
- p35 co-expression targets E-cadherin to lysosomes and p35-triggered disappearance of E-cadherin precursor can be blocked specifically by lysosomal protease inhibitors, indicating p35 induces endocytosis and subsequent degradation of precursor E-cadherin
- results indicate that Src and E-cadherin may play an important role in epithelial-mesenchymal transformations, invasion, and aggressive clinicopathologic features of head and neck squamous carcinoma
- E-cadherin expressioni in adenomas suggest that this molecule might have role in adenoma formation though not necessarily be involved in neoplastic progression.
- ASH1 inactivates DKK1 and DKK3, negative regulators of Wnt/beta-catenin signaling, E-cadherin, and integrin beta1 through ASH1-mediated deacetylation and repressive trimethylation of lysine 27 of histone H3 in the promoter regions of DKK1 and E-cadherin.
- No CDH1 polymorphisms or haplotypes were associated with GC risk, no differences of effect were seen by H pylori infection. Three CDH1 polymorphisms in the same haplotype interacted with smoking to increase GC risk in smokers but not in never smokers.
- The heterotypic trans-interaction of LI- and E-cadherin might play a role during development of the intestinal epithelium when the cells do not yet have elaborate membrane specializations.
- Methylation of CDH1 was present in 80% of NSCLC tissues but only in 14% of noncancerous tissues.
- Activin A downregulates E-cadherin expression in endometrial cells.
- This study provides into the mechanisms underlying the functional role of EZH2 overexpression in gastric cancer cells and a new modality of regulation of E-cadherin expression in silencing mechanisms of tumor suppressor genes.
- Positive staining for E-cadherin should not preclude a diagnosis of lobular in favor of ductal carcinoma.
- Cdh1 may act as an important component in tumor suppression and could be considered as a novel biomarker in breast cancer.
- The -160A, 234 2I allele and haplotype A-A-T-2I were risk factors of Transitional Cell Carcinoma of the Bladder. Haplotype C-A-T-I might act as a protective factor for TCCB.
- transforming growth factor-beta1 indirectly reduces antigen-presenting cell density in EpM by affecting E-cadherin expression, which might explain the increased susceptibility of abnormal tissue differentiation.
- superficial intramucosal signet ring carcinoma, although widespread, is predominantly located in the proximal one third of the stomach in patients with E-cadherin gene mutations.
- Data show that the haplotype the E-cadherin gene may have impact on the risk of epithelial ovarian carcinoma. The CC genotype of 3'-UTR + 54CT may be a potential risk factor for the epithelial ovarian carcinoma.
- study of correlation between mutations & expression of E-cadherin, beta-catenin, occludin & claudin & complexity of colon carcinoma growth; perturbed expression & distribution of these proteins was found, but could not be linked to complexity of growth
- loss of expression of the miR-200 family members may play a critical role in the repression of E-cadherin by ZEB1 and ZEB2 during EMT, thereby enhancing migration and invasion during cancer progression.
- Rsults suggest that the lower epithelial alpha-catenin, E-cadherin and (or) ZO-1 expression in patients with atopic asthma contributes to a defective airway epithelial barrier and a higher influx of eosinophils in the epithelium.
- The nonsense-mediated-decay mRNA surveillance pathway downregulates aberrant E-cadherin transcripts in gastric cancer cells and in CDH1 mutation carriers.
- ADAM15 catalyzes the cleavage of E-cadherin to generate a soluble fragment that in turn binds to and stimulates ErbB receptor signaling
- aberrant or decreased expression of E-cadherin seems to be one of most promising markers of poor prognosis in localized prostate cancer
- promoter-hypermethylation of E-cad is significantly associated with its defective expression and tumor differentiation in non-small cell lung cancer
- Reduced expression of E-cadherin may have a role to play in the pathogenesis of invasive Paget's disease of the vulva.
- The CDH1 163+37235G>A polymorphism may represent a novel susceptibility variant for sporadic diffuse gastric cancer
- E-cadherin loss in tumors contributes to metastatic dissemination by inducing wide-ranging transcriptional and functional changes
- N-glycosylation at Asn-633 is essential for E-cadherin expression, folding and trafficking.
- results indicate that E-cadherin in the nevus cells of the giant congenital nevocellular nevi may affect nevus cell motility rather than intercellular attachment
- data did not support a crucial role of promoter methylation of the E-cadherin gene in the remarkable downregulation of E-cadherin expression in colorectal cancers
- E-cadherine and CD44 immunoexpression in oral squamous cell carcinoma as prognosis factors.
- Loss of E-cadherin-mediated adhesion led to acquisition of phenotypic properties that augmented cell motility and directed transition from precancer to cancer in skin-like tissues.
- loss of E-cadherin is probably consequent on p120 loss or decrease. Aberrations and other alterations of the E-cadherin gene are unlikely to be responsible for the loss of E-cadherin in solid pseudopapillary tumors.
- Results suggest that a decrease in E-cadherin gene expression level in high-grade neuroepithelial tumors may be a hallmark of malignancy in dedifferentiated tumors and that it may be possibly correlated with their progression and dissemination.
- Loss of e-cadherin is associated with ovarian carcinoma
- E-cadherin may have a role in inhibition melanoma invasiveness by epigallocatechin-3-gallate
- Time-lapse microscopy in live cells showed that the recycling endosome is always requisite for E-cadherin sorting and trafficking.
- Results suggest that histone H3 deacetylation plays a crucial role in transcriptional repression of E-cadherin in colorectal cancers.
- rather than being translocated to the nucleus for regulating the target gene transcription, Smad7-stabilized-beta-catenin is shunted to the E-cadherin complex to modulate cell-cell adhesion.
- Rb depletion results in deregulation of E-cadherin.
- The Matrix Metalloproteinase (MMP-2, MMP-9) to E-cadherin (M/E ratio) characterizes an important aspect of the molecular phenotype associated with the histologic progression of prostate cancer among African American prostate cancer patients.
- Results show that InlA triggers two successive E-cadherin post-translational modifications, the Src-mediated tyrosine phosphorylation of E-cadherin followed by its ubiquitination by the ubiquitin-ligase Hakai.
- Hypermethylation of E-cadherin was found in 28 of 38 nasopharyngeal carcinoma
- Sequence analysis of the high-frequency region along E-cadherin exons 7-9 revealed a number of sequence alterations in the patient group as a whole. A C insertion at nt 76,598 was found in 2 African American patients.
- Decreased immunoexpression of beta-catenin and E-cadherin in serous ovarian tumors may be helpful in identifying the cases of higher metastatic potential and infiltration ability.
- Results show a correlation of CDH1 and APC promoter methylation with loss of E-cadherin and APC proteins and with activation of Wnt/beta-catenin signaling pathway.
- beta-catenin expression was significantly related to E-cadherin and MMP-7 expression
- Increased dysadherin expression is possibly one of the post-transcriptional mechanisms responsible for E-cadherin downregulation in thyroid papillary neoplasia.
- The significant difference in methylation of CDHE observed in liver neoplasms and liver cirrhosis was not observed in plasma samples.
- hypermethylation of CDH1 and integrin alpha4 genes may be used as recurrence-associated prognostic indicators in stage I and stage II esophageal squamous cell carcinoma, respectively.
- important role of the E-cadherin/beta-catenin/Tcf signaling pathway in atherosclerosis.
- In the gastric cancerous tissues, the expression percentage of Wnt-1, beta-catenin and E-cadherin is 54.4%, 45.6%, 47.2%, respectively, which is significantly higher than the percentage expression of these genes in normal tissues (p<0.01).
- Patients who had tumors with CDH1 hypermethylation had significantly better overall survival compared with patients who had tumors without hypermethylation (P < .02; log-rank test)
- cadherin-mediated cell-cell contact regulates early keratinocyte differentiation independently from changes in cell shape
- Cdh1-dependent degradation of FoxM1 is required to shut down transcriptional activation of mitotic regulators during exit from mitosis.
- The -347del allele of E-cadherin strongly links with the +178T and +234 13N ins alleles. The -347del/del genotype may increase susceptibility of sporadic gastric carcinoma among males in high-risk areas of China.
- study demonstrated that E-cadherin missense mutants are subjected to Endoplasmic Reticulum Quality Control (ERQC) and that their loss is due to endoplasmic reticulum-associated degradation
- ILK silencing inhibited binding of PARP-1 to SIRE
- Overall meta-analysis indicated that the -160A allele carriers (CA+AA) had a 21% elevated risk of prostate cancer, when compared with the homozygotes (CC) (OR=1.21; 95% CI: 0.97-1.51; P=0.090, Pheterogeneity=0.001).
- the activated AR can downregulate E-cadherin expression to promote the activation of epithelial-mesenchymal transition and tumor metastasis.
- Discontinuous staining of N-cadherin and loss of E-cadherin expression in hepatocellular carcinoma predicts a high risk of recurrence after surgical treatment.
- In human HCC tissues, we observed a correlation among ROS induction, E-cadherin down-regulation, Snail up-regulation, and E-cadherin promoter methylation.
- The presence of E-cadherin in tumors correlated with the absence of metastases in regional lymph nodes and was observed, as a rule, in the patients at the early stages of the disease.
- Activated Akt seems to characterize well-differentiated invasive squamous laryngeal carcinomas, loss of E-cadherin and activation of beta-catenin correlated with high grade carcinomas.
- Tbx2 and Tbx3 may play a dual role during the radial to vertical growth phase transition by both inhibiting senescence via repression of p21(CIP1) expression, and enhancing melanoma invasiveness by decreasing E-cadherin levels.
- In hepatocellular carcinoma (HCC), there is a negative correlation between the positive expression of p130Cas and the normal expression of E-cadherin/beta-catenin. p130Cas plays important roles in the invasion, metastasis and prognosis of HCC.
- Tissue and urine expression of E-cadherin in bladder transitional cell carcinoma are very closely associated with the biological behavior of the neoplasm.
- E-cadherin confer significantly different characteristics on cells.
- E-cadherin plays an important role in uterine receptivity.
- Reduced Cdh1 levels have no effect on destruction of many APC/C substrates during mitotic exit but strongly and specifically stabilize Aurora kinases.
- We suggest that CDH1 cytoplasmic immunolocalization as a result of increased IGF-II levels identifies those nonmuscle invasive presentations most likely to recur
- The resistance of E-cadherin over-expressing cells to staurosporine may due to the up-regulation of Bcl-2/Bax ratio. When E-cadherin interference plasmids were transfected into MCF-7 cells, Bcl-2 expression was down-regulated.
- recruitment of E-cadherin expression by Connexin 43 and inhibits the malignant behaviour of lung cancer cells
- The C-160A polymorphism is not associated with gastric cancer risk in the Italian population.
- overexpression of SRF in colorectal carcinoma cells is associated with modulation of E-cadherin/beta-catenin expression and may play an important role in colorectal cancer metastasis.
- alterations in beta-catenin/E-cadherin complex play a critical role in spindle and/or corded (SPICO) cells' features
- There was increased expression of E-cadherin and beta-catenin in the eutopic and ectopic endometrium in adenomyosis.
- of promoter hypermethylation of TIMP3, CDH1, DAPK, RASSF1A, p16INK4A and MGMT, only the epigenetic silencing of TIMP3 and CDH1 predicted a better outcome in head and neck squamous cell carcinoma
- E-cadherin deficiency initiates gastric signet-ring cell carcinoma in mice and man.