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Updated: Jun 14, 2026

Modeling Hepatitis B Virus Infection in Non-Hepatic 293T-NE-3NRs Cells
Published on: June 5, 2020
[Effect of hepatitis B virus X gene on the apoptosis of HepG2 cells]
Ren-Xian Tang1, Hong-Li Shi, Bao-Feng Fan
1Department of Biological Pathogens, Xuzhou Medical College, Xuzhou 221002, China.
Objective:
To investigate the effect of hepatitis B virus X gene on the apoptosis in X gene-transfected HepG2 cells.
Methods:
HBX gene eukaryon expression vector pcDNA3.1-X was transfected into HepG2 cells by lipid-mediated transfection to establish HepG2/HBX cell model for HBX expression. HepG2 transfected with pcDNA3.1 was used as controls. At 24 h, 48 h, 72 h and 96 h after transfection, cell apoptotic rates were detected by flow cytometry. RT-PCR and Western blot were applied to evaluate the expression levels of HBX, Fas, FasL, and the levels of p-JNK and p-c-Jun protein.
Results:
HBX mRNA was detected in HepG2/ HBX cells 24 h after transfection, and the expression of HBX mRNA level was gradually up-regulated after transfection (P < 0.05); whereas no expression of HBX gene in the control cells. At 24 h, 48 h, 72 h and 96 h after transfection, all of the apoptotic rate in HepG2/HBX group were much higher than those in the controls (P < 0.05). The expression levels of Fas and FasL protein as well as the levels of p-JNK and p-c-Jun protein were significantly higher than those in the controls (P < 0.05). A positive correlationship was observed between the expression of HBX mRNA level and the hepatocyte apoptotic rate (P < 0.05), the same correlation of HBX mRNA level with the levels of Fas, FasL, p-JNK and p-c-Jun were also observed. (P < 0.05).
Conclusion:
HBX can induce hepatocyte apoptosis by up-regulating the levels of p-JNK and p-c-Jun to promote the expression of FasL.
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