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Updated: May 3, 2026

Modeling Hepatitis B Virus Infection in Non-Hepatic 293T-NE-3NRs Cells
Published on: June 5, 2020
[Role of autophagy in HepG-2 cells induced by hepatitis B virus x protein]
Peng Wang1, Zhi-wei Wang2, Hai-xin Qian
1Department of Hepatobiliary Surgery,Affiliated Hospital of Nantong University, Nantong 226000, China.
Objective:
To investigate the role of autophagy in the injury of HepG-2 cells induced by hepatitis B virus x protein (HBx).
Methods:
After HBx transfection, the cells were used to detect the formation of autophagosomes and observed by transmission electron microscopy, monodansylcadaverine (MDC) staining autophagic vacuole (AV), immunofluorescent ce staining microtubule-associated protein light chain 3 ( MAP1-LC3 ) protein, and Western blotting examining the ratio of LC3-II/LC3-I (gray level: 0.760 ± 0.078 vs 0.520 ± 0.086, P < 0.05), beclin 1 (gray level: 0.875 ± 0.093 vs 0.220 ± 0.087, P < 0.05)and lysosome associated membrane protein 2a ( lamp2a ) protein (gray level: 0.320 ± 0.061 vs 0.120 ± 0.064, P < 0.05) levels.
Results:
(1) HBx transfected upregulated the expression of LC3-II, LC3-I, beclin 1 and lamp2a protein. (2) HBx transfected brought about an increase in the formation of autophagosomes and autolysosomes.
Conclusion:
HBx activates the autophagic lysosome pathway in HepG-2 cells through the LC3/beclin1 pathway.
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