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Validated All-in-One™ qPCR Primer for PTEN(NM_000314.6) Search again
Product ID:
HQP088485
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
10q23del, BZS, CWS1, DEC, GLM2, MHAM, MMAC1, PTEN1, PTENbeta, TEP1
Gene Description:
phosphatase and tensin homolog
Target Gene Accession:
NM_000314.6(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 was identified as a tumor suppressor that is mutated in a large number of cancers at high frequency. The protein encoded this gene is a phosphatidylinositol-3,4,5-trisphosphate 3-phosphatase. It contains a tensin like domain as well as a catalytic domain similar to that of the dual specificity protein tyrosine phosphatases. Unlike most of the protein tyrosine phosphatases, this protein preferentially dephosphorylates phosphoinositide substrates. It negatively regulates intracellular levels of phosphatidylinositol-3,4,5-trisphosphate in cells and functions as a tumor suppressor by negatively regulating AKT/PKB signaling pathway. [provided by RefSeq].
Gene References into function
- PTEN mutations are uncommon in Proteus syndrome
- PTEN protects p53 from survival signals, permitting p53 to function as a guardian of the genome. By virtue of its capacity to protect p53, PTEN can sensitize tumor cells to chemotherapy that relies on p53 activity
- novel germline mutation of the PTEN gene in a patient with macrocephaly, ventricular dilatation, and features of VATER association
- modulates vascular endothelial growth factor-mediated signaling and angiogenic effects
- blockage of tumor necrosis factors-induced NF-kappa B-dependent transcription by inhibiting transactivation potential of the p65 subunit
- Germline PTEN mutations have not been identified nor has linkage to 10p21 been demonstrated in 8 subjects with Birt-Hogg-Dube (BHD) syndrome, suggesting that PTEN should be excluded as a candidate gene for BHD.
- PTEN mutations are associated with endometrial carcinomas and hyperplasia
- Mutations in endometrial cancer are the consequence of mismatch repair deficiencies in HNPCC-related cases, but may precede them in sporadic cases.
- expression reduced in pancreatic cancer may give tumor cells growth advantage and contribute to aggressive phenotype
- Review: form and function in human syndromes
- Abnormalities of the PTEN gene are associated with tumor progression, metastasis, and survival.
- Promoter analysis of PTEN:identification of minimum promoter region
- reversible inactivation by hydrogen peroxide
- The phosphatidylinositol phosphatase PTEN is under control of costimulation and regulates proliferation in human T cells. PTEN negatively controls costimulatory signals by antagonizing PI3 K activity in the absence of TCR engagement.
- data suggest that PTEN expression is frequently reduced in advanced breast cancers
- Results show that 9 out of 10 carcinomas exhibited some degree of staining for Akt or PTEN, while normal tissue showed no staining. Akt and PTEN may be diagnostic markers for lung carcinoma.
- PTEN normally is subjected to a feedback mechanism of regulation aimed at maintaining homeostatic levels of D3-phosphoinositides, which are crucial for T cell survival and activation.
- The tumor-suppressive function of Pten depends on its lipid phosphatase activity which disrupts PI-3K/Akt signaling. Loss/mutation of Pten is a marker for poor prognosis in gliomas.
- An Arg234Gln missense PTEN mutation from a patient with multiple brain tumors can't induce apoptosis and leads to high PKB/Akt activation & cell proliferation.
- down regulation of PTEN is associated with HCV-positive cirrhotic hepatocarcinogenesis and increased expression of iNOS and COXII
- role in the pathogenesis of epithelial thyroid neoplasias - review
- PTEN potently inhibited the growth and reduced the size of Jurkat cells. The growth-suppressive effect of PTEN was associated with its ability to induce apoptotic cell death with little or no effect on cell cycle.
- PTEN modulates angiogenesis in prostate cancer by regulating VEGF expression.
- PTEN alterations are late genetic events in the progression of low to high-grade astrocytomas.
- search for potential PTEN modulators through protein-protein interaction
- PTEN may play a critical role in regulating cellular signaling in prostate cancer cells
- PTEN mutations were detected in ILC (truncating mutations) in around 2% of the tumors
- PTEN silencing in anaplastic thyroid cancer is a result of a wide variety of epigenetic and/or structural silencing mechanisms rather than a consequence of structural biallelic inactivation of the classical type.
- PTEN expression in endometrial neoplasms
- These results suggest that PTEN controls mammary gland development and, consequently, lactation.
- used mass spectrometric methods to identify Ser(370) and Ser(385) as in vivo phosphorylation sites of PTEN
- cell growth control by PTEN and it's ability to regulate known cell size regulators involved in protein translation (review)
- there are high frequencies of somatic mutations in PTEN (encoding phosphate and tensin homolog) in breast neoplastic epithelium and stroma
- PTEN suppresses hyaluronic acid-induced matrix metalloproteinase-9 expression in U87MG glioblastoma cells through focal adhesion kinase dephosphorylation.
- A patient with Cowden Disease and all family members exhibited the same 4-bp deletion in exon 8 of the PTEN gene.
- induction of Skp2 may be causally linked with decreased levels of p27 in prostate cancer and implicate PTEN in the regulation of Skp2 expression
- PTEN gene was deleted or weakly expressed in primary renal significant cell carcinoma, which is probably related to tumorigenesis and development of renal cell carcinoma.
- PTEN inactivation may be important for the propagation of melanoma cells in culture, and that another chromosome 10 tumour suppressor gene may be important for melanoma pathogenesis.
- REVIEW: the cellular mechanisms of PTEN and MTMR function and their role in the etiology of cancer and other human diseases
- loss or reduced expression of PTEN protein occures commonly in tumorigenesis and progression of gastric carcinoma
- restoration of PTEN function in gliomas may induce therapeutic effect by downregulating VEGF.
- Mutation and epidermal growth factor receptor activation regulate vascular endothelial growth factor mRNA expression in human glioblastoma cells by transactivating the proximal VEGF promoter.
- Results suggest that activation of peroxisome proliferative activated receptor gamma (PPARgamma) may represent a novel approach for the treatment of pancreatic cancer by increasing PTEN levels and inhibiting PI3K activity.
- Nuclear PTEN varies throughout the cell cycle. Higher nuclear PTEN levels were associated with G0-G1 phase, and lower nuclear PTEN levels were associated with S phase.
- Frequent monoallelic deletion of PTEN and its reciprocal associatioin with PIK3CA amplification is associated with gastric carcinoma
- PTEN/MMAC1 gene mutation is a rare event in soft tissue sarcomas without specific balanced translocations.
- Dysregulated PTEN-PKB and negative receptor status in human breast cancer
- BMP2 exposure can regulate PTEN protein levels by decreasing PTEN's association with the degradative pathway
- Loss of PTEN expression and increased levels of HIF-1alpha and VEGF may play an important role in carcinogenesis and progression of colorectal adenocarcinoma.
- PTEN and p27Kip1 have roles in tumor cell proliferation, and increased risk of recurrence
- overexpression of RRM1 in human and mouse lung cancer cell lines induced PTEN expression, reduced phosphorylation of focal adhesion kinase (FAK), suppressed migration, invasion, and metastasis formation, and increased survival in an animal model.
- study suggests mutations of the PTEN/MMAC1 gene do not occur at a significant rate in advanced gastric carcinoma, but the rare clustered mutation site (exons 2-6) suggests that PTEN/MMAC1 might contribute to gastric carcinogenesis and its progression
- In certain tumor subtypes, PTEN/MMAC1 gene alteration may be useful clinically in the evaluation of the tumor.
- functional role of PTEN in the molecular pathogenesis of prostatic disease [review]
- exposure to Zn2+ ions causes PTEN degradation and loss of function, which is mediated by an ubiquitin-associated proteolytic process in the airway epithelium
- Loss of this protein in EGF receptor-expressing tumor cells counteracts the antitumor action of EGFR tyrosine kinase inhibitors.
- Data suggest that PTEN tumor suppressor gene malfunction seems to be involved in metastasing capacity of hepatocellular carcinoma.
- existence of a regulatory mechanism of protein stability and PTEN-protein interactions during apoptosis, executed by caspase-3 in a PTEN phosphorylation-regulated manner.
- PTEN modulates IGF-2-mediated signaling. The phosphoprotein phosphatase activity of PTEN downregulates IGF-2 expression in hepatoma cells.
- phosphorylation/dephosphorylation of the C-terminal region of PTEN serves as an electrostatic switch that controls the membrane translocation of the protein
- PTEN has a novel germ-line mutation in a PHTS patient with a granular cell tumor.
- Hepatitis B X protein in liver cells down-regulates the expression of PTEN and activates AKT.
- Germline PTEN promoter mutations and deletions in Cowden/Bannayan-Riley-Ruvalcaba syndrome result in aberrant PTEN protein and dysregulation of the phosphoinositol-3-kinase/Akt pathway.
- a PI(4,5)P2 monomer binds to PTEN, initiates an allosteric conformational change and, thereby, activates PTEN independent of membrane binding
- activated Src inhibits PTEN function leading to alterations in signaling through the PI3K/AKT pathway
- The data are consistent with an oncogenesis model in which a lack of PTEN fuels the cell cycle by increasing the nuclear availability of cyclin D1 through the Akt/PKB pathway.
- Down-regulated expression of PTEN plays important role in tumorigenesis, progression, growth, differentiation, and angiogenesis of gastric cancer. Low expression of PTEN can decrease expression of caspase-3 to disorder apoptosis of tumor cells.
- tumor suppressor PTEN, inhibits the interaction of CH-ILKBP with ILK
- Down-regulated PTEN expression and up-regulated MMP-7 expression were greatly implicated in tumorigenesis and progression of gastric carcinoma.
- The survival data on 129 glioblasstoma patients were correlated with the results of a detailed analysis of this gene.
- Oxidative stress activates PI 3-kinase-dependent signalling via the inactivation of PTEN.
- ovarian cancer PTEN does not play a major role in disease progression and is not involved in the alteration of p27Kip1 expression
- ovarian steroids regulate the endometrial PTEN pool
- PTEN inhibits MDM2 and protects p53 through both p13k/Akt-dependent and -independent pathways in ALL.
- PTEN has a role in anchorage-independent colony formation and anchorage-dependent proliferation
- loss of PTEN function is sufficient to cause Lhermitte-Duclos disease
- Mutation in PTEN is associated with Bannayan-Riley-Ruvalcaba syndrome
- TNF-alpha-induced down-regulation of PTEN is mediated through a TNF-alpha/NIK/NF-kappaB pathway.
- The results indicate that the evaluation of PTEN mutation are useful to predict dissemination and prognosis of glioblastomas.
- These data also suggest that location of intragenic PTEN mutations and their coexistence with the CMYC amplification may play a crucial part in the development of various subtypes of endometrial carcinoma.
- Loss of PTEN expression is common and correlates with tumor progression and lymph node metastasis in breast carcinoma.
- Lipid rafts(LR) may play important role in determining function of PI 3-K/Akt2 signaling, including stimulation of intestinal Na absorption. LR-associated Akt2 may be involved in enterocyte differentiation.
- A conserved N-terminal motif of PTEN is needed for correct membrane orientation, cellular activity and tumour-suppressor function.
- importance of PTEN in primary sporadic colorectal cancer: PTEN gene mutations in 19.5% (8/41) of tumours and allele loss, including all or part of the PTEN gene, in a further 17% (7/41) of the cases
- regulates cell proliferation and apoptosis through inhibition of IGF-IR synthesis
- results show that PTEN can inhibit cell migration through its C2 domain, independent of its lipid phosphatase activity; ability of PTEN to control cell migration through its C2 domain is likely to be an important feature of its tumor suppressor activity
- Loss of PTEN gene not uncommon in NSCLC, but level of PTEN protein expression is not an independent prognostic marker in early-stage NSCLC.
- possible cooperation between BRAF activation and PTEN loss in melanoma development.
- PTEN downregulation is implied in GIST progression.
- PTEN is regulated by anionic lipids and reactive oxygen species [review]
- a tumour suppressor candidate protein binds to extreme C-terminal region of PTEN and regulates PTEN protein turnover [review]
- PTEN mutations were detected in 7 cases (14.3%) of synovial sarcoma, and all of these were monophasic tumors
- Hypermethylation of the PTEN promoter correlated significantly with either decreased or complete loss of PTEN protein expression in colorectal cancer.
- a role of these tumor suppressor and metastasis suppressor genes in the evolution and progression of NSCLC
- PTEN mutation is associated with HPV-negative adenocarcinoma of the uterine cervix
- PTEN methylation and loss of PTEN expression are early events in the development of cervical cancer and may have prognostic significance.
- PTEN, via distinct mechanisms, differentially regulates androgen receptors in various stages of prostate cancers.
- One common way of stimulating the 1-Phosphatidylinositol 3-Kinase kinase pathway occurs through inactivation of the PTEN tumor suppressor
- Modification of the Egr-1-dependent mechanisms may play a role in the silencing of PTEN gene expression occurring during thyroid cell transformation.
- We found that indomethacin and NS-398 treatment significantly upregulated expression of the tumor suppressor gene, PTEN.
- Inhibitory effects of PTEN on cell motility translate into suppression of in vivo invasion.
- PTEN promoter hypermethylation is a common event in sporadic breast cancer, correlating with other well-established prognostic factors of this malignancy
- PICT-1 (protein interacting with carboxyl terminus 1) binds to the C terminus of PTEN and regulates its phosphorylation and turnover.
- Methylation of the PTEN promoter leads to PTEN inactivation in a subset of human breast cancers
- PTEN mRNA and protein expression as well as PTEN-related cell growth inhibition in endometrial cancer cells.
- inactivation of PTEN gene and over-expression of VEGF contribute to the neovascularization and progression of gastric cancer
- PTEN acts in T cells primarily to control basal PI-3,4,5-P3 levels, rather than opposing PI3K acutely during TCR stimulation.
- PTEN expression was a strong predictor of both, shorter relapse-free survival and shorter disease-specific survival.
- Data show that PTEN and MXI1 were two candidate tumor suppressor genes on 10q23 and 10q24-q25 and may be potentially involved in the initiation and progression of prostate carcinoma.
- in contrast to prostate cancer, mutations in the PTEN gene seem not to affect cellular distribution of the beta-catenin protein in endometrial carcinomas.
- The Tumor suppressor PTEN was involved in control of VEGF/VEGFR-2 stimulated prostate cancer cell adhesion as well as proliferation.
- findings expand our understanding of tumor promoter/suppressor inter-relationships and downstream transcriptional effects of PTEN loss and c-Met overexpression in malignant gliomas
- PTEN expression in the initial steps of the apoptotic pathway is regulated by EGR-1
- the function of the PTEN gene in hepatocarcinomas may be impaired mainly through point mutations and expression deficiency; and the defect of PTEN in tumor cells may alter the phosphorylation of FAK.
- reactive oxygen species generated by insulin stimulation contributes to the inactivation of PTEN and not to the activation of PI-3 kinase in the PI-3 kinase/Akt pathway
- Dysregulation of the PI 3-K/AKT/PTEN pathway may contribute to early head neck squamous cell carcinoma tumorigenesis.
- reduced PTEN expression may be an independent prognostic indicator in patients with invasive ductal carcinoma.
- PTEN has a role in regulating actin polymerization but not directionality during mammalian cell chemotaxis
- Overexpression of human PTEN in rat vascular smooth muscle cells inhibits the cellular processes necessary for neointimal hyperplasia. PTEN is a critical regulator of cell growth in the vasculature.
- Review. PTEN removal of the phosphate from PtdIns(3,4,5)P(3) inhibits the PI3-kinase/Akt pathway, preventing localisation of pleckstrin homology domain proteins to the cell membrane. Alterations of PTEN are associated with cancer & other diseases.
- Increase of PTEN expression in ethanol-exposed cells is the main causative factor in altering the balance between prosurvival and prodeath signals initiated by TNF.
- PTEN mutations are restricted to advanced gastric cancer, loss of heterozygosity and mutation of PTEN gene are closely related to the infiltration and metastasis of gastric cancer.
- Alterations in beta-catenin and PTEN genes, as well as MSI, are frequent in low-stage ovarian carcinomas of endometrioid type that have a favorable prognosis.
- Intratubular germ cell neoplasias intensely expressed PTEN, indicating that loss of PTEN expression is not an early event in testicular tumor development.
- Sod2 can serve as an alternative physiological source of the potent signaling molecule, H2O2 via PTEN oxidation
- Transient and near-complete loss of PTEN expression induces loss of adhesion of the cells.
- loss of PTEN and subsequent activation of AKT impair CHK1 through phosphorylation, ubiquitination, and reduced nuclear localization to promote genomic instability in tumor cells
- May be susceptible to dimethyl sulfoxide, shich might therefore be an antineoplastic agent.
- Dimethylsulfoxide induced upregulation of PTEN in HL-60 leukemia cells.
- S1P2R receptor actively regulates the PTEN phosphatase by a Rho GTPase-dependent pathway to inhibit cell migration.
- Data show that DJ-1 is a key negative regulator of PTEN that may be a useful prognostic marker for cancer.
- the regulation of PTEN expression may play an important role in the development of the early gestational trophoblast and in the pathogenesis of hydatidiform mole, but not in its malignant transformation
- The PTEN is a phosphatase that dephosphorylates both protein and phosphoinositide substrates.
- EGF and hypoxia induce CXCR4 in non-small cell lung cancer, a process regulated by the PI3-kinase/PTEN/AKT/mTOR signaling pathway and activation of HIF-1alpha
- The PTEN is a phosphatase that dephosphorylates both protein and phosphoinositide substrates.
- Subset of individuals with autism spectrum disorders and extreme macrocephaly associated with germline PTEN tumour suppressor gene mutations
- protection of p53 from MDM2 by PTEN and the damage-induced activation of PTEN by phosphorylated p53 leads to the formation of an apoptotic amplification cycle in which p53 and PTEN coordinately increase cellular apoptosis
- expression of PTEN increases during terminal follicular growth
- the present results suggest that PTEN expression may be a useful indicator of cell proliferation in patients with STS.
- We demonstrate that the expression of the tumor suppressor gene PTEN has a significant inverse correlation with fatty acid synthase (FAS) expression in prostate cancer, and inhibition of the PTEN gene leads to the overexpression of FAS in vitro.
- Activated AKT was associated with increased resistance to multiple chemotherapeutic agents in gastric cancer.
- loss of PTEN expression is the first biomarker in endometrial intraepithelial neoplasia that increases the accuracy of the prognostic morphometric D score to predict cancer progression risk.
- the C-terminal region of PTEN in is important for the selective association with scaffolding and/or regulatory molecules and PDZ domain binding stabilizes PTEN and targets it for phosphorylation by microtubule-associated serine/threonine kinases
- The colocalization of sphingomyelinases, ceramide, polyphosphoinositides, and PTEN in the raft fraction further suggests that the association of these lipids is critical for regulating cell death
- PTEN protein could inhibit cell invasion even in the presence of the constitutively active epidermal growth factor receptor(EGFR)
- We identified the dual phosphatase and tumor suppressor protein PTEN as an LKB1-interacting protein.PTEN is a substrate of kinase LKB1 in vitro.
- PTEN contributes to G1 growth arrest through an Akt-independent signaling pathway.
- PTEN expression negatively regulates chemotaxis of lymphoid mammalian cells via its lipid phosphatase activity
- Study demonstrated that PTEN-positive and phosphorylated-Akt-negative expression was a predictor of survival for patients with advanced endometrial carcinoma.
- Reduced expression of PTEN protein correlated with lymph node metastases in the patients with breast cancer
- PTEN expression is down-regulated in HCC cell lines probably due to loss of activity of PTEN promoter.
- PTEN represses RNA Pol I transcription through a novel mechanism that involves disruption of the SL1 complex
- sequestration of PTEN in the cytoplasm likely limits PTEN nuclear translocation
- Notch homolog 1 can participate in cross-talk with other signaling pathways such as Ras/Raf/MEK/ERK through the regulation of the PTEN tumor suppressor
- multiple kinases, including CK2 and GSK3beta, participate in PTEN phosphorylation and GSK3beta may provide feedback regulation of PTEN
- Data on loss of heterozygosity at specific loci on chromosomes 10q, 9p, and 17p and PTEN mutations on exons 5 and 6 indicated their role in glioma progression in Malay population.
- the clinical data linking IGFBP-2 expression to poor prognosis may arise, at least in part, because high levels of IGFBP-2 expression correlate with loss of function of PTEN
- Inhibition of PTEN expression in fibroblasts may contribute to the pathogenesis of fibrotic lung disease.
- loss of Pten is more frequent in anaplastic large cell lymphoma as compared to other mature T-/NK-cell lymphomas, which strongly correlates with the loss of cyclin-dependent kinase inhibitor 1B expression
- 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.
- The alteration of the PTEN gene may be associated with malignant transformation of ovarian epithelial tumors. The PTEN gene seems to be a negative regulator of cell proliferation in ovarian adenocarcinomas.
- CKIepsilon-induced down-regulation of PI3K/Akt signaling through PTEN leads to amplified sensitivity to apoptosis.
- Together, these studies demonstrate a novel signal transduction pathway involving p38MAPK-NF-kappaB-PTEN in IL-18-mediated HCMEC death, and identify IL-18 as potential therapeutic target to inhibit or reduce myocardial inflammation and injury.
- Results suggest that the PTEN gene may be involved in the etiology of both smoking initiation and nicotine dependence.
- SEL1L modulates the expression of the matrix metalloproteinase inhibitors TIMP1, TIMP2 and the PTEN gene
- alterations in ROS levels contribute to macrophage homeostasis by altering the balance between PI 3-kinase/Akt and the phosphatase, PTEN
- SPRY2 mediates its anti-proliferative actions by altering PTEN content and activity
- Resistin induces PTEN expression by activating stress signaling p38 pathway, which may activate target transcription factor ATF-2, which in turn induces PTEN expression
- PTEN loss is correlated with substantial increases in Akt(Ser473) and integrin-linked kinase expression, both of which promote Ser(9) phospho-inhibition of GSK3beta and inactivation of apoptotic factors
- data provide clues to understand regulation of PTEN expression and possible mechanisms of pathogenesis of subset of Cowden syndrome individuals with germ line promoter variation and who lack mutations in PTEN coding region and splice sites
- Data suggest that PTEN may regulate the expression of p27 by negatively regulating S phase kinase-associated protein 2 expression.
- Pten has a role in prostate cancer progression
- The differential expression of PTEN and its splice variants could play a role in the pathogenesis of sporadic breast neoplasms and Cowden disease.
- Our observations suggest potential prognostic significance of p185(HER2) overexpression with PTEN loss in gastric adenocarcinoma patients. This opens up the possibility of considering p185(HER2)and PTEN as a therapeutic target in gastric cancer.
- these results show a high frequency of PTEN promoter hypermethylation, especially in follicular tumors, suggesting its possible role in thyroid tumorigenesis
- PTEN inactivation may play a role in progression to an androgen independence (AI) stage of advanced prostate cancer.
- Multiple PTEN mutations in the same tumor were more frequent in tumors with microsatellite instability.
- Results suggest that the altered PTEN expression and its inverse correlation with survivin may be involved in the development and progression of ovarian tumors.
- Survivin is positively correlated with PTEN expression in gastric cancer; PTEN expression is a molecular marker of advanced gastric cancer
- The dynamic membrane association could be modulated temporally or spatially to alter PTEN activity in specific physiological situations and could have important implications for tumor suppressor function.
- OPN acts downstream of PI3K in melanoma and PTEN loss contributes to melanoma development
- PTEN functions as a key regulator of mast cell homeostasis and FcepsilonRI-responsiveness
- PTEN induction confers androgen independent CaP cells enhanced responsiveness to the anti-proliferative effects of anti-androgens and this action may involve non-AR mediated effects.
- eukaryotic translation initiation factor 4E binding protein 1(4E-BP1) overexpression is associated with prostate cancer, especially when combined with phosphatase and tensin homolog(PTEN) and mammalian target of rapamycin(mTOR) expression data
- The data demonstrate that c-Jun contributes to the promotion of cellular survival by regulating the expression of PTEN.
- The negative expression of PTEN in ovarian endometriosis without atypia (EN), ovarian endometriosis with atypia (EA), and endometriosis with adjacent ovarian carcinoma (ET) is a manifestation of the inactivation of this gene.
- PTEN loss causes reduced NKX3.1 expression in both murine and human prostate cancers.
- These genetic and translational observations establish a cooperative role of Pten and Ink4a/Arf in the development of HS and provide mechanistic insights into the pathogenesis of human HS.
- Loss of heterozygosity is an independent prognostic factor and PTEN is a candidate as a haploinsufficient tumor suppressor in gastric cancers.
- activation of the PI3K/AKT pathway constitutes an important step in the molecular pathogenesis of medulloblastoma and that dysregulation of PTEN may play a significant role in this context
- modulation of PTEN inactivation may also occur at the transcription level influencing the specific phenotypes seen in Cowden and Bannayan-Riley-Ruvalcaba syndromes
- Multiple nuclear exclusion motifs and a nuclear localization domain control PTEN nuclear localization by a Ran-dependent mechanism and suggest a proapoptotic role for PTEN in the cell nucleus.
- Microsatellite instability (MSI) leading to the functional inactivation of the PTEN gene has also been reported for ovarian adenocarcinomas with frequencies varying from 6 to 37%.
- Epigenetic PTEN silencing seems to be a relevant mechanism of inactivating this tumor suppressor gene in melanoma that may promote melanoma development by derepression of the AKT pathway.
- PC12 and U251 cells overexpressing PTEN had decreases in adrenomedullin mRNA levels. Cellular and secreted adrenomedullin peptide was similarly reduced. U251 cells overexpressing PTEN did not respond to exogenous adrenomedullin.
- SHIP2 substitutes for PTEN in the acute regulation of PKB in PC3 cells but not other prostate cell lines, where PTEN may share this role with further PIP3-degrading mechanisms.
- These results provide further evidence that nuclear PTEN plays a role through cell cycle suppression functions in regulating carcinogenesis.
- REVIEW: current view of the interaction of PTEN with the plasma membrane and what the implications are for cancer biology
- findings demonstrate that PTEN potently modulates hepatitis B virus-X protein-mediated signaling
- Combination therapy provides added benefit in promoting cell death in PTEN-deficient tumor cells.
- Acetylation promotes p53 tetramerization, which, in turn, is required for the PTEN-p53 interaction and subsequent maintenance of high p53 acetylation.
- The high frequency of PTEN deletion observed in CaP versus precursor lesions implicates a pivotal role for PTEN haploinsufficiency in the transition from preneoplastic PIN to CaP.
- results confirm that PIK3CA mutations are frequent in endometrial carcinoma and support the hypothesis that PIK3CA mutations may have an additive effect to PTEN monoallelic inactivation in endometrial carcinoma
- In advanced bladder cancers, PTEN protein was significantly reduced by initiating transitional cell carcinoma and promoting progresssion.
- collagen matrix contraction activates PTEN by a mechanism involving cytoskeletal disassembly
- Data show that UVB irradiation increases PTEN/Akt phosphorylation in dermal fibroblasts, and inhibition of PTEN and activation of Akt by phosphorylation are involved in UVB-induced MMP-1 and -3 secretions through upregulation of AP-1 activity.
- AdPTEN strongly inhibits the growth of human prostate tumors, especially when combined with radiation therapy, and that this effect is mediated by the induction of apoptosis, and by the inhibition of angiogenesis and cellular proliferation.
- PTEN mRNA levels were significantly lower in the glioma tissues than in the benign brain tumors and tumor-adjacent normal tissues, whereas there were no statistical differences between benign brain tumor and the tumor-adjacent normal tissues.
- Akt activ correlates with HER2 overexpr or LOH at the PTEN gene locus while inversely correlating with PR expression. When LOH at the PTEN gene locus and HER2 overexpr occurred simultaneously, incidence of Akt activ and reduced PR expr was significant
- report on the first somatic mutation of a tumor-suppressor gene, PTEN, in Focal cortical dysplasias with Taylor-type balloon cells
- took a haplotype-based approach and investigated the association of specific genomic regions of the PTEN locus with PTEN hamartoma tumor syndrome
- PTEN nonsense mutation in a Bannayan-Riley-Ruvalcaba syndrome family disrupts a potential exonic splicing enhancer and causes exon skipping
- Activation of PI3K signaling by mutations in PTEN or PIK3CA can lead to activation of p53-mediated growth suppression. phosphatidylinositol (3,4,5)-triphosphate-induced mitogenesis during human cancer pathogenesis.
- PTEN mutations were significantly correlated with uterine endometrioid carcinoma compared with atypical hyperplasia.
- Altered phosphorylation of PTEN protein and the consequent activation of survival signals may contribute to the pathomechanism of leiomyoma.
- Cooperation between this gene and BMPR1A gene is deleted on chromoome 10 in juvenile polyposis coli.
- Our results indicate that Ad-PTEN exerts its tumor suppressive effect on bladder cancer cells through inhibiting survivin and upregulating caspase-related proteins. Thus Ad-PTEN may be potentially therapeutic for the treatment of bladder cancers.
- In conclusion, using a biologically relevant model system to dissect PTEN tumor suppressor function in human bladder cancer, we identified three molecules important for many cellular functions in complex with PTEN.
- determinatin of types and frequencies of PTEN gene alterations in Turkish patients with glioblastoma multiforme & relationship between alterations of the gene & histopathological properties; mutations may have an effect on aggressiveness of GBM tumors
- PTEN reportedly interacts in vitro with the EF hand-like motif of major vault protein in a Ca(2+)-dependent manner in a breast tumor cell line.
- NEDD4-1 is a potential proto-oncogene that negatively regulates PTEN via ubiquitination, a paradigm analogous to that of Mdm2 and p53.
- Nuclear PTEN is essential for tumor suppression and that PTEN nuclear import is mediated by its monoubiquitination.
- These results demonstrate that PTEN plays a fundamental role in the maintenance of chromosomal stability through the physical interaction with centromeres and control of DNA repair.
- We conclude that most frequently occurring mutations in the PTEN gene may be a key event for the tumorigenesis of endometrioid endometrial carcinomas.
- These data indicate that the aberrant expression of PTEN contributes to the activation of the PI3kinase/Akt pathway and its transcription factor mediators in glioma.
- PTEN tumor-suppressor protein has a role in response to epidermal growth factor receptor tyrosine kinase inhibitors in glioblastoma
- PTEN acts as an anti-inflammatory protein to prevent neointima formation in an animal model of arterial injury.
- p21 plays a key role in mechanisms used by PTEN-deficient tumors to escape chemotherapy
- Alterations in PTEN and amplification of EGFR are uncommon in pediatric malignant gliomas, in contrast to adult malignant gliomas.
- TNF-alpha induces upregulation of PTEN expression through NF-kappaB activation in human leukemic cells
- Results further affirmed the role of this element in PTEN's regulation and deregulation, and its contribution to the pathogenesis of Cowden syndrome.
- loss of PTEN function in human prostate cancer may specifically facilitate bone rather than other organ metastasis and suggest that Rac1, as a PTEN effector, may contribute to this metastatic tropism.
- PTEN could be a good prognostic factor for lung carcinomas, regardless of the histological types.
- IGF-II and IGFBP-2 differentially regulate PTEN in human breast cancer cells
- PTEN and IGFBP-2 expression are inversely correlated in human brain and prostate cancers
- Comparative genomic hybridization and immunohistochemical assessment of EGFR, PTEN, p53, and MIB-1 expression in 13 oligodendrogliomas, one oligoastrocytoma and 23 high-grade astrocytomas is reported.
- bi-allelic inactivation of PTEN can lead to developmental anomalies instead of malignant transformation, thus raising the question of the limitations of the tumor suppressive function in this gene.
- Exogenous PTEN gene induces apoptosis in breast carcinoma cell line MDA468.
- Increased PTEN expression in unstimulated MCF-7 breast cancer cells results in a 51% increase in phosphatidic acid, with a decrease in phosphatidylcholine, suggesting that PTEN may regulate phospholipase D and phospholipase C.
- GAL-3 mediates TRAIL signaling by regulating PTEN in human breast carcinoma cells
- PTEN mutations are a relatively infrequent cause of autism spectrum disorders with macrocephaly.
- PTEN/PI 3-kinase signaling and cyclin D1 control a novel pathway that regulates assembly of the SCF(SKP2) complex.
- A model in which the phosphorylation of Thr366 plays a role in destabilizing the PTEN protein is reported.
- Up-regulation of PTEN at the transcriptional level is an advers prognostic factor in female lung adenocarcinomas.
- aberrant PI3K pathway signaling is strongly associated with metastasis and poor survival across carcinoma types
- findings show that unconjugated bilirubin modulates a signaling pathway involving APE1/Ref-1, Egr-1, and PTEN
- PPARgamma and RAR play an important role in controlling the growth of leukemia cells via the up-regulation of PTEN
- In Ishikawa H cells that model type I endometrial cancer in the loss of PTEN and RB1, re-expressing PTEN and RB1 increased the apoptotic and G1 phases and decreased the S and G2-M phases, which further sensitize the cells to gefitinib.
- Loss of PTEN may also be associated with a worse prognosis in patients with early-stage endometrial carcinoma.
- methylation of the PTEN promoter may represent an alternate mechanism by which PI3K signaling is increased in grade II and III gliomas as well as secondary GBMs
- Vascular anomalies in patients with a PTEN mutation are typically multifocal intramuscular combinations of fast-flow channels and ectopic fat; cerebral developmental venous anomalies are very common
- It is unlikely that the EMX2 or PTEN gene variants investigated contribute to risk for initiation and/or development of endometriosis.
- the COOH-terminal tail can act as an autoinhibitory domain to control both PTEN membrane recruitment and phosphatase activity
- PIK3CA mutations and PTEN loss were not mutually exclusive events and associated with similar prognostic factors
- identifies the RhoA/ROCK pathway as a major target of p110delta-mediated PI 3-kinase signalling
- Metastasis of renal cell carcinoma is correlated with inactivation of PTEN.
- loss of PTEN expression, together with increased Akt phosphorylation, contributes to progression and recurrence of prostate cancer
- PTEN expression in leukemic blasts may be correlated with risk of relapse and survival
- IKK alpha controls mTOR kinase activity in Akt-active, PTEN-null prostate cancer cells, with less involvement by IKK beta
- PTEN germline mutations are rare
- Pten inactivation has a role in emergence of androgen-independent prostate cancer [review]
- transcriptional down-regulation of the tumor suppressor PTEN in pancreatic adenocarcinoma if facilitated by effect of K-RAS/ERK on TGFbeta
- Mutations in PTEN is asociated with clear cell sarcoma of the kidney
- PIK3CA mutations are mutually exclusive with PTEN loss in diffuse large B-cell lymphoma
- results suggest that the induction of PTEN-modulated apoptosis is one of the putative mechanisms of tumor suppressive activity by GLTSCR2
- Increased promoter methylation of PTEN was present in renal metastasis (of breast cancer), coinciding with the decrease in the level of normal PTEN transcript
- Aberrant expression of miR-21 can contribute to hepatocellular carcinoma growth and spread by modulating PTEN expression and PTEN-dependent pathways.
- PTEN dominantly inhibits Akt activation, the coexistence of high levels of the PTEN protein with enhanced Akt activation suggests the existence of novel mechanisms which attenuate PTEN
- The up-regulation of PTEN inhibited Akt and MDM2, which enhanced the level of p53, thereby inducing G(2)/M arrest and apoptosis.
- Findings suggest that the JNK/PTEN and NF-kappaB/PTEN pathways play a critical role in normal intestinal homeostasis and colon carcinogenesis.
- Data indicates that haploinsufficiency or PTEN genomic loss is an indicator of more advanced disease at surgery, and is predictive of a shorter time to biochemical recurrence of disease.
- decreased protein expressions due to increased MMAC gene mutation in advanced endometriosis and ovarian cancers were not observed; a significant difference in MMAC immunostaining between endometriosis and ovarian endometriod adenocarcinoma was seen
- REsults describe PTEN and NDUFB8 aberrations in cervical cancer tissue.
- Aberrant location of expression/staining intensity of PTEN, PPM1A and P-Smad2 in hepatocellular carcinoma may impact disease progression.
- These data show that PTEN plays a non-redundant role in EGF-induced chemotaxis of human breast cancer cells, and an optimal level of PTEN is required in these responses.
- Genetic alterations of chromosome 10q23, including the PTEN gene, could be important in hepatocarcinogenesis
- Inhibition of PI3K signaling by PTEN inhibits tumor angiogenesis and growth. AKT is the downstream target of PI3K in controlling angiogenesis and tumor growth.
- Loss of PTEN expression in Jurkat T cells does not impact on the PDK-1/PKC pathway and that only a subset of kinases, such as PKB/Akt, are perturbed as a consequence PTEN loss.
- (PTEN) functions as a phosphoinositide 3-phosphatase, that antagonizes phosphatidylinositol 3-kinase --{REVIEW}
- Altogether, our results suggested that E-cadherin mediated cell-cell adhesion was essential for preventing the proteasome degradation of PTEN.
- examined the downstream effect of five PTEN promoter variants (-861G/T, -853C/G, -834C/T, -798G/C, and -764G/A) that are not within any known cis-acting regulatory elements
- TLX recruits histone deacetylases to repress transcription of p21(CIP1/WAF1) and pten and regulate neural stem cell proliferation
- 2 point mutations in PTEN (697C>T & 253 +1G>T)were associated with juvenile polyposis syndrome.
- Mutational loss of PTEN induces resistance to NOTCH1 inhibition in T-cell leukemia.
- hyperglycemia triggers apoptosis by inhibiting Akt signaling via ONOO(-)-mediated LKB1-dependent PTEN activation
- PTEN plays a critical role in MAGI-2-induced inhibition of cell migration and proliferation in human hepatocarcinoma cells
- A reduction in PTEN expression appears to be an early step in renal cell carcinogenesis. However, the PTEN expression pattern of renal cell carcinomas apparently is not prognostic for patient survival.
- In patients with mycosis fungoides, several loci associated with the tumor suppressor gene PTEN on chromosome 10 appear to be associated with progression from plaque to tumor stage.
- PTEN deficiency has a role in trastuzumab resistance, which can be reversed by combinations of trastuzumab with triciribine or RAD001
- In breast cancer stem-like cells, the STAT3 pathway was found to be positively regulated by mTOR signaling, whereas PTEN served as a negative regulator of both STAT3 and mTOR signaling.
- Western blot analysis showed that six out of 25 (24%) lung cancer cell lines displayed low expression of PTEN protein.
- loss of PTEN expression was significantly associated with sentinel lymph node micro-metastasis
- High levels of p-AKT expression occurred independently of the presence of PTEN or PIK3CA mutations in endometrial cancer.
- Cell cycle progression from the G(1) to the S phase is arrested in cells expressing wild-type PTEN, suggesting a role for PTEN as a tumor suppressor gene.
- In trastuzumab-treated breast cancer patients combined analysis of PTEN and PIK3CA identified twice as many patients at increased risk for progression compared to PTEN alone.
- the loss of PTEN protein expression is associated with nonresponsiveness to cetuximab.
- PTEN expression is infrequent in ovarian carcinoma
- Analysis of PTEN gene mutations may be useful for characterization of the molecular event in hepatic angiosarcoma and cancer predisposition.
- PTEN may play an important role in carcinogenesis and the progression of esophageal squamous cell carcinoma in a high incidence area of northern China, and PTEN could serve as an important factor to predict clinical outcome and prognosis
- The PTEN is crucial onvolement in neuronal injury as well as in neurological and psychiatric disorders.
- These findings imply that oncogenic Ras suppresses the apoptotic gene PTEN via the Raf-MEK-ERK-c-Jun pathway to induce antiapoptosis and cellular transformation.
- Combination of PTEN/p53/PCNA represent an independent prognostic factor for tumor recurrence and disease-specific survival in hepatocellular carcinoma after surgery.
- there is a reciprocal regulation between PI3K and PTEN that defines a novel negative-feedback loop in cell cycle progression
- BMP2 downregulates PTEN via RAS/ERK in a SMAD4-null environment that contributes to cell growth, and constitutes a SMAD4-independent but BMP-responsive signaling pathway.
- Upregulation of sterol response element-binding protein (SREBP), known to induce PPARgamma expression, can increase PTEN expression.
- Study shows that loss of PTEN expression is significantly associated with the basal-like breast cancer subtype in human sporadic and BRCA1-associated hereditary breast cancers.
- Down-regulated expression of FHIT and PTEN may contribute to gastric carcinogenesis possibly by involving in the imbalance between apoptosis and proliferation of cells.
- Large genomic deletions of SMAD4, BMPR1A and PTEN are a common cause of JPS.
- combined analysis of Cdx2 and nuclear PTEN expression can have significant value in distinguishing histological types of gastric cancer and assessing prognosis in patients with gastric cancer.
- miR-214 induces cell survival and cisplatin resistance primarily through targeting the PTEN/Akt pathway.
- Mammalian target of rapamycin is the key effector of phosphatidylinositol-3-OH-initiated proliferative signals in the thyroid follicular epithelium in PTEN mutant mice.
- Nuclear PTEN plays a role in chromosome stability, DNA repair, cell cycle arrest and cellular stability. The balance between these functions is an important factor in determining whether a cell remains benign or becomes neoplastic.
- PTEN binds to membranes through multiple sites, but only PI(4,5)P2 binding to the N-terminal domain triggers a conformational change with increased alpha-helicity
- frequency of the occurrence of BRAF mutation and/or RET/PTC in H4-PTEN positive tumors was extremely high (75%) in papillary thyroid carcinoma
- In pancreatic tumor cells calcium-dependent PKC-alpha mediates TGF-beta-induced transcriptional downregulation of PTEN, and this pathway promotes cell migration in a SMAD4-null environment.
- The loss of PTEN was shown to lead to increased levels of ARF4L protein but no change in transcript levels. The ARF4L transcript preferentially localized to the polysomal compartment after PTEN loss in glioma.
- The population of tumor cells with monosomy of chromosome 10 and PTEN locus correlated significantly with histological grade. High-grade astrocytomas (AAs and GBMs) had elevated fractions of tumor cells with monosomy of chromosome 10 and PTEN locus.
- Results discuss the role of PTEN upon the E3 ubquitin ligase Nedd4 as a negative feedback regulator as well as a substrate.
- the regulation of PTEN,phosphatase and tensin homolog gene expression .
- APE1 regulated PTEN expression is mediated by Egr-1.
- Mutations in the key residues which control PTEN lipid and protein phosphatase may act as dominant-negative mutants to suppress endogenous PTEN and alter the sensitivity of breast cancer patients to chemo- and targeted therapies.
- the expression manner of PTEN, beta-catenin, and p53 immunocytochemistry was observed in the normal endometrium (proliferative, secretory, and atrophic, and endometrial glandular and stromal breakdown
- the expression manner of PTEN, beta-catenin, and p53 immunocytochemistry was observed in the normal endometrium (proliferative, secretory, and atrophic, and endometrial glandular and stromal breakdown[beta-catenin]
- PTEN acquires unexpected properties by enhancing gain-of-function mutant p53 (mut-p53) protein levels. PTEN restoration to cells harboring mut-p53 leads to induction of G(1)-S cell cycle progression and cell proliferation and to inhibition of cell death.
- constitutive activation of Akt correlates with the expression of the phosphorylated, inactive form of PTEN
- Development of endometrial carcinoma is associated with an overexpression of NDRG1 and the loss of PTEN expression.
- Increased PTEN expression was associated with invasive adenocarcinoma of the prostate
- our observations suggest that GW501516 induces the proliferation of NSCLC cells by inhibiting the expression of PTEN through activation of PPARbeta/delta, which stimulates PI3K/Akt and NF-kappaB signaling.
- PTEN represses RNA polymerase III-dependent transcription by targeting the TFIIIB complex
- Enhanced insulin signaling in Pten deficiency suppresses autophagy at the formation and maturation steps of autophagosomes.
- PTEN and p27Kip1 are not downregulated in the majority of renal cell carcinomas
- germline PTEN mutation is associated with Hamartoma Tumor Syndrome
- New epigenetic mechanism that genistein reactivates the expression of PTEN and the majority of nuclear antagonists of NF-B by modulating either histone H3-Lysine 9 (H3-K9) methylation or deacetylation leading to inhibition of the AKT signaling pathway.
- Gene deletions in the PTEN gene are associated with Cowden disease.
- differential expression of PTEN-targeting miR-19a and miR-21 modulates the PTEN protein levels and the CS and CSL phenotypes, irrespective of the patient's mutation status, and support their roles as genetic modifiers in CS and CSL.
- VHL mutation alone is insufficient for tumor formation; study shows that epididymal cystadenomas from VHL patients frequently also lack expression of the PTEN tumor suppressor and display activation of phosphatidylinositol 3-kinase pathway signaling.
- PTEN abrogates TGF-beta-induced Smad2/3 phosphorylation. This study establishes a novel role for nuclear PTEN in the stabilization of PPM1A.
- Down-regulation of PTEN expression via methylation is associated with oral squamous cell carcinoma
- patients with 10q23 microdeletions involving the PTEN and BMPR1A genes have variable clinical phenotypes, which cannot be explained merely by the deletion sizes, and are not restricted to severe infantile juvenile polyposis
- Deficient PTEN expression is associated with worse overall survival in high-grade gliomas
- Loss of PTEN function is insufficient to adequately predict responsiveness to mTOR inhibitors in glioblastoma multiforme.
- mTOR signaling pathway is activated in two endometrial carcinoma cell strains and the status of activation is related with PTEN expression of the cells
- ATP regulates PTEN subcellular localization in breast, colon and thyroid cancer cell lines.
- 1) PAK plays a required role in hyperosmotic signaling through the PI3K/pTEN/Cdc42/PP2Calpha/p38 pathway, and 2) PAK and PP2Calpha modulate the effects of this pathway on focal adhesion dynamics.
- First report of Cowden syndrome presenting with ovarian dysgerminoma, which implicates PTEN in the molecular pathogenesis of dysgerminoma and adds it to the phenotypic manifestations of Cowden syndrome.
- Cellular resistance to TRAIL could be developed through phosphorylation (activation) of Akt and phosphorylation (inactivation) of PTEN in acute lymphoblastic leukemia cells.
- PTEN gene mutation and expression may play an important role in the occurrence and development of gastric cancer.
- Necrosis and hemorrhage were associated with PTEN expression
- PTEN is expressed in endometrium as it progresses to endometrial carcinoma
- Adiponectin blocks interleukin-18-mediated endothelial cell death via APPL1-dependent AMP-activated protein kinase (AMPK) activation and IKK/NF-kappaB/PTEN suppression.
- These findings indicate that PTEN plays an important role in the coordinated induction of apoptosis and G(1) arrest by carnosic acid and arsenic trioxide.
- Data suggest that alteration of PTEN may upregulate NDRG1, which may be an important gene in facilitating endometrium carcinogenesis.
- results demonstrated that PTEN had played an important role in the cell proliferation, cell migration and invasion dependent on its phosphatase activity
- KRAS mutations and PI3KCA/PTEN deregulation significantly correlate with resistance to cetuximab.
- PIK3CA mutations, in comparison with PTEN loss and AKT1 mutations, were associated with significantly less and inconsistent activation of AKT and of downstream PI3K/AKT signaling in tumors and cell lines
- CSIG acts as a novel regulatory component of replicative senescence, which requires PTEN as a mediator and involves in a translational regulatory mechanism.
- Lack of PTEN gene amplification was associated with more responses to cetuximab and longer time to progression in coloretal cancers.
- in prostate cancer cells at least two mechanisms of drug resistance are interconnected. PTEN and mTOR signaling were shown: to be involved into regulation of MRP1 and BCRP
- coexpression of PTEN and AR should be undertaken to validate this pilot study and the utility of these biomarkers in routine histopathologic workup of patients with PC
- results delineate a previously unknown PML-DAXX-HAUSP molecular network controlling PTEN deubiquitinylation and trafficking, which is perturbed by oncogenic cues in human cancer
- Chk1 is phosphorylated at Ser(317) by ATR resulting in stabilization of CKII, which in turn leads to phosphorylation of PTEN at Thr(383).
- report a statistically significant lower expression intensity of PTEN and HePTP and higher nuclear SHP2 expression
- Although p110alpha activation is required to sustain the proliferation of established PIK3CA-mutant tumors, PTEN-deficient tumors are dependent instead on p110beta signaling.
- PTEN mutations were seen concomitantly with FGFR2 mutations
- Lys(402) acetylation modulates PTEN interaction with PDZ domain-containing proteins, indicating a potential role of acetylation in regulating PTEN function
- impairment of function in senescent ECs in culture is mediated by an increase in S1P signaling through S1P(2)-mediated activation of the lipid phosphatase PTEN
- PTEN is mutated in a significant subgroup of colorectal carcinomas, and all novel mutations found were in tumors harboring wild-type TP53.
- findings show mTOR is targeted for ubiquitination & degradation by binding to FBXW7; breast cancer cell lines & primary tumors showed a reciprocal relation between loss of FBXW7 & deletion or mutation of PTEN, which also activates mTOR
- The characterization of PTEN and PTEN-related pathways from a multidisciplinary perspective underscores the importance of incorporating data from different -omics, which is crucial for the advancement of personalized medicine.
- Mechanisms by which PTEN maintains genomic stability.
- The diverse ways in which PTEN signaling is modified in cancer.
- Total PTEN was absent in 33.3% of ameloblastomas, while its stabilized, phosphorylated(ser380 / thr382 / thr383) form was absent in 83.3% of tumors.
- PTEN posttranslational inactivation and hyperacivation of the PI3K/Akt pathway sustain primary T cell leukemia.
- Aberrant methylation and hence silencing of the PTEN gene coexisting with activating genetic alterations of the PI3K/AKT pathway is associated with thyroid tumors.
- a role for both cytoplasmic and nuclear PTEN in progression of prostate cancer to the hormone-refractory state
- PTEN upregulation is responsible for Pfn1-dependent attenuation of AKT activation in MDA-MB-231 cells.
- Myc as an important target for cooperative actions of p53 and Pten in the regulation of normal and malignant stem/progenitor cell differentiation, self-renewal and tumorigenic potential
- Reduced PTEN expression was detected in more than one third of ovarian clear cell adenocarcinoma cases. Neither PTEN promoter methylation nor LOH at 10q23 locus is significantly related to PTEN inactivation and is not an adverse prognostic factor in OCCA
- the consequence of PTEN loss and Akt2 overexpression function synergistically to promote metastasis
- PTEN influences Fas signaling, at least in part, by regulating PEA-15 phosphorylation and activity that, in turn, regulate the ability of Bcl-2 to suppress Fas-induced apoptosis.
- A hypothetical model whereby PTEN loss upregulates cell cycle genes such as cdc6 and cyclin E2 that in turn promote metastatic colonization at distant sites.
- PTEN membrane binding requires PIP(2) and phosphorylation regulates an intramolecular interaction.
- the PTEN/PI3K/Akt pathways are critical for prostate cancer stem-like cell maintenance
- Results show that transformed human prostate epithelial cells lacking PTEN require mTORC2 to form tumors when injected into nude mice.
- PTEN loss amplifies c-Met-induced glioblastoma malignancy.
- Deletion of Pten transgene in adult neural stem cells (NSCs) is not tumorigenic but promotes NSC expansion; perturbation of PTEN-phosphatidylinositol 3-kinase (PI3K) pathway alone in NSCs is not tumorigenic.