Hepatitis B virus x protein promote human hepatocellular carcinoma cells proliferation by activating p38 and JNK signalling pathway

Abstract

Objective To investigate the effects and mechanism of hepatitis B virus x protein (HBx) on human hepatocellular carcinoma cells proliferation. Methods Eukaryotic expression vector HBx-pEGFP-C1 was constructed. HepG2 cells were transfected transiently using Lipofectamine 2000. HBx expression in transfected cells were measured by RT-PCR and Western blot. Cells proliferation and apoptosis were detected by using growth curves and TUNEL staining. The protein levels of caspase-3, p-p38, p-Akt and p-JNK were measured by Western blot. Results HBx was successfully expressed in HepG2 cells. Growth curve result showed that HBx promoted cell proliferation (t=-0.8999, P=0.012). Compared with control group, the levels of p-p38(24 h) (t=- 11.058, P=0.0004) and p-JNK(48 h) (t=- 15.022, P=0.0001) in HBx-pEGFP-C1 group were increased significantly. There is no significant difference between the two groups′ apoptosis. Conclusions Transient overexpression of HBx promoted human hepatic carcinoma cells proliferation and activated the p38 and JNK signalling pathway. Key words: Hepatitis B virus X protein; HepG2; p38; c-Jun N-terminal kinase