OBJECTIVE: To investigate the roles of the mammalian target of rapamycin-1 and -2 (mTORC1 and TORC2) in the proliferation and apoptosis of prostate cancer 22RV1 cells. METHODS: After silencing mTORC1 and TORC2, we examined the proliferation and apoptosis of prostate cancer 22RV1 cells by methylthiazol tetrazolium (MTT) assay and flow cytometry, respectively, and detected the expressions of the androgen receptor (AR) and Akt phosphorylation in the prostate cancer 22RV1 cells by Western blot after transfecting Raptor-siRNA and Rictor-siRNA to the 22RV1 cells. RESULTS: MTT showed that the prostate cancer 22RV1 cells had no significant change in the growth rate after mTORC1 silence (P > 0.05), but their proliferation was markedly inhibited after mTORC2 silence (P < 0.01). Flow cytometry revealed a dramatic increase in the apoptosis of the 22RV1 cells after mTORC1 silence (P < 0.01), but no obvious change after mTORC2 silence (P > 0.05). Western blot exhibited that mTORC1 silence significantly increased the expression of AR and Akt phosphorylation (P < 0.05), while mTORC2 silence markedly decreased them (P < 0.05). CONCLUSION: mTORC2 is not only required for the survival of prostate cancer 22RV1 cells, but also a promising therapeutic target of prostate cancer.
OBJECTIVE: To investigate the roles of the mammalian target of rapamycin-1 and -2 (mTORC1 and TORC2) in the proliferation and apoptosis of prostate cancer 22RV1 cells. METHODS: After silencing mTORC1 and TORC2, we examined the proliferation and apoptosis of prostate cancer 22RV1 cells by methylthiazol tetrazolium (MTT) assay and flow cytometry, respectively, and detected the expressions of the androgen receptor (AR) and Akt phosphorylation in the prostate cancer 22RV1 cells by Western blot after transfecting Raptor-siRNA and Rictor-siRNA to the 22RV1 cells. RESULTS:MTT showed that the prostate cancer 22RV1 cells had no significant change in the growth rate after mTORC1 silence (P > 0.05), but their proliferation was markedly inhibited after mTORC2 silence (P < 0.01). Flow cytometry revealed a dramatic increase in the apoptosis of the 22RV1 cells after mTORC1 silence (P < 0.01), but no obvious change after mTORC2 silence (P > 0.05). Western blot exhibited that mTORC1 silence significantly increased the expression of AR and Akt phosphorylation (P < 0.05), while mTORC2 silence markedly decreased them (P < 0.05). CONCLUSION:mTORC2 is not only required for the survival of prostate cancer 22RV1 cells, but also a promising therapeutic target of prostate cancer.