STAT3 promotes the proliferation and migration of hepatocellular carcinoma cells by regulating AKT2.

The aim of the present study was to investigate the correlation of STAT3 and AKT in HCC cells. HCC cells were transfected with si-STAT3 and si-AKT2 in vitro and the mRNA expression of STAT3 and AKT was detected by RT-PCR, and the protein expression was measured by western blot. MTT assays were used to evaluate cell proliferation, and Transwell assays were performed to detect the ability of migration and invasion. The relationship between STAT3 and AKT was analyzed by ChIP and Dual-luciferase reporter (DLR) assays. A nude mice experiment was used to verify the correlation. In the present study, we found that the expression of p-AKT2 and its downstream molecules were reduced in HCC cells transfected with si-STAT3, and the expression of p-STAT3 and its downstream molecules was decreased in HCC cells transfected with si-AKT2. Moreover, the ability of HCC cells proliferation, migration and invasion was decreased in si-STAT3 transfection group, but AKT2 reversed the role of si-STAT3 in HCC cells. The ChIP experiment found that STAT3 could bind to the AKT2 promoter in HCC cells. The DLR assay showed that the luciferase activity of AKT2 promoter was enhanced in HCC cells treated by IL-6. The nude mice experiment found that the tumor grew slowly after transfection with the STAT3-siRNA lentiviral vector, while AKT2 reversed the effect. STAT3 and AKT2 had mutual regulatory relationship, and STAT3 promoted the occurrence and development of HCC by regulating AKT2.