[Effects of rapamycin on prostate cancer PC-3 cells].

Abstract

Background and objective: The mammalian target of rapamycin (mTOR) signaling network regulates cell growth, proliferation, survival and apoptosis. This study was to investigate the effect and the underlying mechanism of rapamycin on prostate cancer PC-3 cells.

Methods: PC-3 cells were treated with 1 nmol/L rapamycin. The proliferation of PC-3 was examined by MTT. The cell cycle distribution of PC-3 was measured by FCM. The protein levels of raptor, rictor, Akt, pS6k1-T389, pAkt-s473 in PC-3 were examined by western blot.

Results: Rapamycin increased the proliferation of PC-3 at 24 h, however, it remarkably inhibited cell proliferation after 36 h (P<0.01), which became more obviously at 72 h. Although incubation with rapamycin slightly induced cell arrest at the S phase at 24 h, this gradually increased PC-3 cells at the G1 phase at 36 h and 48 h. Compared with the control group, the protein levels of raptor and pS6k1-T389 were significantly decreased (P<0.01), and those of rictor and Akt remained unchanged after the treatment with rapamycin for 24 h; the protein level of pAkt-s473 was significantly increased at 24 h (P<0.01), but was obviously inhibited at 36 h and almost completely inhibited at 72 h (P<0.01).

Conclusions: Prolonged rapamycin treatment inhibits the proliferation of PC-3 cells. This may be caused by rapamycin-induced cell cycle arrest at the G(1) phase and inhibition of Akt phosphorylation.