MicroRNA-195 regulates docetaxel resistance by targeting clusterin in prostate cancer.

MicroRNAs (miRNAs) have been implicated in neoplasm growth, metastasis, vasculogenesis, and drug resistance. It has been validated that abnormal miR-195 expression was related with poor survival of prostate cancer (PC); however, its role in the resistance to chemotherapeutic drugs docetaxel (DOC) in PC is still acquainted scarcely. In our study, the lower expression of miR-195 was appeared in DOC-resistant PC cells (DU145/DOC) rather than DOC-sensitive DU145 cells. The up-regulation of miR-195 lowered the IC50 of DOC, facilitated the apoptosis and inhibited the colony formation ability in DU145/DOC cells. Moreover, we also found that miR-195 had the binding site with clusterin (CLU) by the online TargetScan database mining. Luciferase tests revealed that miR-195 binds to the 3'-UTR of CLU. MiR-195 overexpression decreased the amassment of CLU in DU145/DOC cells. Knockdown of CLU diminished the IC50 of DOC and enhanced the apoptosis of DU145/DOC cells, which was consistent with the influence of miR-195 on DOC-induced cell apoptosis. Taken together, our results illuminated that miR-195 improved the sensitivity of resistant PC cells to DOC by suppressing CLU. Hence, miR-195 may be a potentially promising molecular target for drug resistance of PC.