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

W. Wang, J. Liu, Q. Wu

Department of Radiation Oncology, Henan Provincial People’s Hospital, ZhengZhou, China. weiwang1980s@tom.com

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• Oncology

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.

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