Cancer cell growth is characterized by reprogrammed glucose metabolism and subsequent high rate of glycolysis. The metabolic reprogramming is essential for cell proliferation and drug resistance of cancer cells including glioblastoma (GBM). MicroRNAs play pivotal roles during GBM development. In the present study, we discovered a significant downregulation of miR-1297 in GBM. Decreased miR-1297 expression was associated with prolonged overall survival of patients with glioma. Overexpression of miR-1297 promoted cell proliferation and glycolysis in GBM cells. Bioinformatic analysis (TargetScan and miRanda) indicated that miR-1297 might target 3'UTR of KPNA2, a key regulator of glycolysis in GBM. The regulation was confirmed in a dual-luciferase reporter assay in GBM cells. Furthermore, overexpression of KPNA2 could reverse miR-1297 mimic induced cell growth arrest and inhibition of glycolysis in GBM cells. Finally, a negative correlation between miR-1297 and KPNA2 mRNA levels was observed in GBM tissues. Collectively, the data demonstrated that the abnormal metabolic reprogramming was driven by miR-1297 in GBM and suggested miR-1297 as a tumor suppressor.
Keywords: Glioblastoma; Glycolysis; KPNA2; miR-1297.