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.
Keywords: miR-183-5p , aerobic glycolysis, migration, invasion, PTEN/Akt/mTOR, hepatocellular carcinoma