Co-occurrence of this pathogenic germline mutation in <i>PTEN</i> in this patient, early development of OCCC at age 28 years, and total loss of PTEN expression in the tumor might support the involvement of <i>PTEN</i> in the carcinogenesis of her ovarian cancer.
In addition, compared with cells over-expressed SIRT6, cell apoptosis was repressed and cell proliferation and tumorigenesis were enhanced in cells with SIRT6 over-expression and PTEN knockdown.
The meta-analysis indicated a significantly increased risk of tumorigenesis in the PTEN low-level group relative to the control group (OR = 0.098, 95% CIs: 0.067-0.143, P < 0.001).
Further experiments demonstrated that the expression levels of PTEN and phosphorylated-AKT in HEC-1B and Ishikawa endometrial cancer cells was decreased and increased, respectively, following aberrant expression of miR-423. miR-423 displayed an important role in tumorigenesis and progression in endometrial cancer cells, and may therefore be used as a potential biomarker to predict chemotherapy response and prognosis in endometrial cancer.
These results suggest that the mechanism underlying <i>H. pylori</i>-induced carcinogenesis may involve promoting cell invasion through the phosphorylation of PTEN and the activation of FAK.
Although the regulation of these two pathways occurs in the same hepatocyte, the details of crosstalk between Hippo-YAP/TAZ and PTEN-AKT pathways in liver homeostasis and tumorigenesis still remain unclear.
Therefore, how PTEN lipid phosphatase inactivation contributes to the occurrence and development of gastric cancer and the potential role of the Hippo and PI3K/Akt pathways in PTEN lipid phosphatase inactivation mediated gastric tumorigenesis remain to be explored.
At the membrane, PTEN functions as a phosphatidylinositol (3,4,5)-trisphosphate phosphatase and suppresses PI 3-kinase signaling that drives cell growth and tumorigenesis.
Studies examining PTEN and ERG simultaneously found these genes are likely to occur together, but cooperative tumorigenesis functions have not been conclusively established.
1 alpha,25-dihydroxyvitamin D<sub>3</sub> (1,23(OH)<sub>2</sub> D<sub>3</sub>) is known to play a dual role in cancer, by promoting or inhibiting carcinogenesis via 1,23(OH)<sub>2</sub> D<sub>3</sub> receptor (VDR) and phosphatase and tensin homolog deleted on chromosome 10 (PTEN).
Together, these findings provide a novel model to study the mechanism of fallopian tube tumor initiation and invasion to the ovary mediated by loss of PTEN, which may help to define early events of human ovarian carcinogenesis.
Ablation of phosphatase and tensin homolog (PTEN) or the protein kinase Hippo signaling pathway induces liver cancer via activation of AKT or the transcriptional regulators YAP/TAZ, respectively; however, the potential for crosstalk between the PTEN/AKT and Hippo/YAP/TAZ pathways in liver tumorigenesis has thus far remained unclear.
We also identify a new exon 2b in GOLGA2 transcript and the exon exclusion contributes to PTEN knockdown-induced tumorigenesis by promoting dramatic Golgi extension and secretion, and PTEN depletion significantly sensitizes cancer cells to secretion inhibitors brefeldin A and golgicide A.
Taken together, these data suggest that genes other than ERG and PTEN may drive carcinogenesis/progression in the majority of men with germline HOXB13 mutations.