ASPP2 inhibits hepatitis B virus replication by preventing nucleus translocation of HSF1 and attenuating the transactivation of ATG7

Hepatitis B virus (HBV) is a kind of virus with the capability to induce autophagy, thereby facilitating its replication. Reducing hepatocyte autophagy is proved to be a useful way to inhibit HBV replication. Herein, we reported that p53‐binding protein 2 (apoptosis‐stimulating protein of p53‐2, ASP...

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Detalles Bibliográficos
Autores principales: Wang, Shanshan, Sun, Yu, Wang, Yang, Wang, Anna, Kou, Buxin, Che, Yang, Chen, Dexi, Zhang, Yulin, Shi, Ying
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2021
Materias:
Original Articles
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8278078/
https://www.ncbi.nlm.nih.gov/pubmed/34085409
http://dx.doi.org/10.1111/jcmm.16699
Descripción
Sumario:Hepatitis B virus (HBV) is a kind of virus with the capability to induce autophagy, thereby facilitating its replication. Reducing hepatocyte autophagy is proved to be a useful way to inhibit HBV replication. Herein, we reported that p53‐binding protein 2 (apoptosis‐stimulating protein of p53‐2, ASPP2) could attenuate HBV‐induced hepatocyte autophagy in a p53‐independent manner. Mechanistically, overexpressed ASPP2 binds to HSF1 in cytoplasm of HBV‐infected cells, which prevents the translocation of HSF1 to nuclei, thereby inhibiting the transactivation of Atg7. By regulating the transcription of Atg7, ASPP2 reduces hepatocyte autophagy, thereby inhibiting HBV replication. Therefore, ASPP2 is a key regulator of cell autophagy, and overexpression of ASPP2 could be a novel method to inhibit HBV replication in hepatocytes.

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