miR-183-5p Promotes HCC Migration/Invasion via Increasing Aerobic Glycolysis

Abstract

Background The mortality and morbidity of hepatocellular carcinoma (HCC) are still unacceptably high, despite decades of extensive studies. Aerobic glycolysis is a hallmark of cancer metabolism, closely relating to invasion and metastasis of HCC. MicroRNAs (miRNAs) are involved in the regulation of aerobic glycolysis. miR-183-5p, an oncogenic miRNA, is highly expressed in HCC, but the regulatory mechanism of miR-183-5p in migration, invasion and aerobic glycolysis in HCC remains unclear. Purpose To elucidate whether miR-183-5p affects aerobic glycolysis to regulate the migration and invasion of HCC, and to explore its regulatory mechanism. Methods We attempted to observe the effects of miR-183-5p on the migration and invasion of HepG2 cells by a wound-healing assay and Transwell assays. The effect of miR-183-5p on glycolysis was determined by glucose uptake and lactate generation. Western blot and qPCR were used to detect the relevant proteins and miRNA expression. Results Our results show that miR-183-5p promoted migration and invasion, enhanced glycolysis via increasing glucose uptake and lactate generation, and up-regulated glycolysis-related gene (PKM2, HK2, LDHA, GLUT1) expression in HepG2 cells. Further experiments indicated that miR-183-5p could decrease PTEN expression, but increased Akt, p-Akt and mTOR expression in HepG2 cells. Conclusion These findings suggest that miR-183-5p may promote HCC migration and invasion via increasing aerobic glycolysis through targeting PTEN and then activating Akt/mTOR signaling.