Downregulated microRNA-26a modulates prostate cancer cell proliferation and apoptosis by targeting COX-2.

MicroRNA-26a (miR-26a) is expressed at lower levels in prostate cancer cells compared with normal prostate cells. However, the regulatory mechanism of miR-26a in tumorigenesis and metastasis is not clear. In the present study, the expression profile of cellular miR-26a was analyzed by reverse transcription-quantitative polymerase chain reaction. The potential target of miR-26a was identified by luciferase assay and western blotting. Examination of miR-26a function was performed by transfection with miR-26a mimics and inhibitor. It was found that miR-26a expression was decreased in prostate cancer tissues and cell lines, with androgen-independent prostate cancer (AIPC) showing lower miR-26a expression compared with androgen-dependent prostate cancer (ADPC). Overexpression of miR-26a by transfecting miR-26a mimics could significantly enhance apoptosis, and this upregulation of apoptosis was triggered by cytochrome c oxidase subunit II inhibition. Furthermore, it was found that lower miR-26a density resulted in an evidently poor prognosis. Understanding the important roles of miR-26a in regulating cell apoptosis in human prostate cancer cells may aid the exploration of AIPC transformation mechanisms and contribute to the development of miRNA-based therapy in the future.