Conditional homozygous knockout of PTEN mediated by PAX8-cre recombinase was sufficient to drive endometrioid and serous borderline ovarian carcinoma, providing the first model of FTE-derived borderline tumors.
Overall, we suggest that miR-205 functions as an oncogenic miRNA by directly binding to SMAD4 and PTEN, providing a novel target for the molecular treatment of ovarian cancer.
It is for the purpose of this study to investigate its function and the mechanisms by which PTEN enhances the sensitivity of ovarian cancer to antitumor agents.
Dual targeting of phosphoinositide 3-kinase and mammalian target of rapamycin using NVP-BEZ235 as a novel therapeutic approach in human ovarian carcinoma.
The OC tissues exhibited an increased expression of miR-214 and a reduced positive rate of PTEN expression compared with adjacent normal tissues. miR-214 may activate the PI3K/Akt signaling pathway by downregulating the targeted PTEN, which may promote OC cell proliferation and inhibit apoptosis.
Grb2 depletion under non-stimulated conditions inhibits PTEN, promotes Akt-induced tumor formation and contributes to poor prognosis in ovarian cancer.
The function of miR-222 was detected in ovarian carcinoma to verify the regulation of phosphatase and tensin homolog (PTEN) by miR-222. miR-222 expression in ovarian carcinoma tissues and cell lines were examined using RT-qPCR.
Taken together, these data suggest that PTEN over-expression may represent a novel therapeutic approach for chemoresistant human ovarian cancer and that this may involve a p53-mediated apoptotic cascade independent of the PI3K/Akt pathway.