MiRNA-92a promotes cell proliferation and invasion through binding to KLF4 in glioma.

Abstract

OBJECTIVE: Glioma is one of the most frequent brain tumors in adults, and it has a low 5-year survival rate. MicroRNA-92a (miR-92a) has been reported to be upregulated and acted as an oncogene in many cancers. The purpose of this study was to explore the molecular mechanisms of miR-92a and kruppel-like factor 4 (KLF4) in glioma. PATIENTS AND METHODS: Western blotting assay and quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) were applied to calculate the relative expression of interest proteins and mRNAs. Luciferase ability assay was conducted to evaluate whether miR-92a was targeting to KLF4. RESULTS: A higher expression of miR-92a was observed in glioma tissues compared with the corresponding adjacent non-tumor tissues. The upregulation of miR-92a predicted poor prognostic characteristics of glioma. The overexpression miR-92a significantly promoted cell proliferation an invasion, while the knockdown of miR-92a presented the opposite results. MiR-92a bound to KLF4 and mediated the expression of KLF4 in glioma cells. The knockdown of miR-92a inhibited cell invasion-mediated EMT. Furthermore, the knockdown of miR-92a suppressed cell proliferation through the KLF4/AKT/mTOR signal pathway. CONCLUSIONS: MiR-92a promoted the proliferation through the KLF4/AKT/mTOR signal pathway in glioma. The newly identified miR-92a/KLF4/AKT/mTOR axis provides novel insight into the pathogenesis of glioma.