Hepatitis B virus x protein promote human hepatocellular carcinoma cells proliferation by activating p38 and JNK signalling pathway
10.3760/cma.j.issn.1003-9279.2019.04.013
- VernacularTitle: 乙型肝炎病毒x蛋白通过激活p38和JNK信号通路促进肝癌细胞增殖
- Author:
Xiaoli LOU
1
;
Yanqiang HOU
Author Information
1. Department of Central Laboratory, Shanghai Songjiang District Central Hospital, Shanghai 201600, China
- Publication Type:Journal Article
- Keywords:
Hepatitis B virus X protein;
HepG2;
p38;
c-Jun N-terminal kinase
- From:
Chinese Journal of Experimental and Clinical Virology
2019;33(4):394-399
- CountryChina
- Language:Chinese
-
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.
