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Updated: Sep 19, 2025

siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells
Published on: October 28, 2019
HBV promotes epithelial-mesenchymal transition in HCC and liver fibrosis through JNK-mediated autophagy
Dong Chen1,2, Jian Hong3, Wenting Li2,4
1Center of Hepato-Pancreato-Biliary Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong Province, China.
Background:
HBV, which contributes to liver fibrosis and HCC, is associated with autophagy and epithelial-mesenchymal transition (EMT). However, the relationship between HBV infection, autophagy, and EMT remains unknown.
Methods:
In this study, we used HBV cell lines (HepAD38, Huh7.5.1-NTCP) to evaluate this relationship.
Results:
HBV replication or infection promoted autophagy, EMT, and liver fibrogenesis. HBV-induced EMT/fibrogenesis was dependent on autophagy. HBV X and HBV core (C) were each involved during this process. TGF-β1 partially participated in HBV-induced autophagy/EMT/fibrosis. c-Jun N-terminal kinase (JNK) expression was increased in HepAD38 cells, HBV-X (HBV-C)-transfected Huh7.5.1 cells, and HBV-infected Huh7.5.1-NTCP cells. JNK silencing attenuated HBV-induced autophagy and EMT/fibrosis signaling as well. Moreover, overexpression of HBV-X(C) and augmentation of autophagy were shown to promote pJNK expression. Finally, we confirmed an HBV-JNK-autophagy-EMT/fibrosis signaling pathway in a primary human hepatocyte model.
Conclusions:
In conclusion, HBV induces autophagy through JNK, thus triggering downstream EMT and fibrogenesis signaling pathways. These findings suggest that JNKs could be potential targets for the treatment of HBV-related liver diseases.
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