MiR-205 suppresses autophagy and enhances radiosensitivity of prostate cancer cells by targeting TP53INP1.

OBJECTIVE This study aimed to investigate the role of miR-205 in radiosensitivity and autophagy of prostate cancer cells and to explore its regulative effect on TP53INP1. MATERIALS AND METHODS MiR-205 expression was compared in three prostate cancer cell lines (DU145, PC-3 and LNCaP) and one normal human prostate epithelial cell line (RWPE-1). The effect of irradiation-induced autophagy on radiosensitivity of the cancer cells and the effect of miR-205 on irradiation-induced autophagy were explored. The regulative effect of miR-205 on TP53INP1 and the function of this axis was further studied. RESULTS Ectopic expression of miR-205 substantially reduced the survival fraction of both DU145 and LNCaP cells to irradiation and inhibited irradiation-induced autophagy. Irradiation-induced autophagy acted as a protective mechanism in prostate cancer cells. TP53INP1 is a direct functional target of miR-205 in irradiation-induced autophagy and radiosensitivity regulation. CONCLUSIONS The miR-205/TP53INP1 mediated autophagy pathway might be an important molecular mechanism regulating radiosensitivity of prostate cancer cells and represents a potential therapeutic target for prostate cancer.