MiR-424-5p Inhibits Proliferation, Invasion and Promotes Apoptosis and Predicts Good Prognosis in Glioma by Directly Targeting BFAR.

Abstract

The biological function of miRNA (miR)-424-5p in glioma has not been clarified. This study was to explore the roles of miR-424-5p/Bifunctional apoptosis regulator (BFAR) axis in glioma. Ninety-six pairs of human glioma tissues and their adjacent non-cancer tissues were collected. The levels of BFAR and miR-424-5p were detected by quantitative polymerase chain reaction (qPCR) in glioma tissues and cell lines. Moreover, the biological roles of miR-424-5p and BFAR in glioma cells were assessed. We found a miR-424-5p binding site in the 3'UTR of BFAR by using TargetScan 7.2 online database. The miR-424-5p level was dramatically decreased in glioma tissues and cell lines, and the BFAR expression was significantly increased. The BFAR expression was negatively related to the miR-424-5p level in glioma tissues. Compared to patients with high miR-424-5p levels in glioma tissues, patients with low miR-424-5p levels had significantly lower survival rate (χ2 = 13.728 and P < 0.001). Compared to patients with high BFAR levels in glioma tissues, patients with low BFAR levels had significantly higher survival rate (χ2 = 5.516 and P = 0.027). Furthermore, up-regulation of miR-424-5p obviously restrained glioma cells proliferation and invasion, and promoted apoptosis. Besides, knockdown of BFAR also could markedly inhibit the proliferation and invasion, and promote apoptosis. Finally, overexpression of BFAR in glioma cells partially reversed the inhibited effects of miR-424-5p mimic. Knockdown of miR-424-5p restrained glioma cell apoptosis and promoted invasion and proliferation via regulation of BFAR.