The microRNA‐155 mediates hepatitis B virus replication by reinforcing SOCS1 signalling–induced autophagy
Autor: | Xiao-Ren Wang, Bing-Zhu Yan, Pengfei Yang, Bao-Shan Yang, Man-Ru Bi, Li-Yan Chen, Xiaoyu Ming, Wensong Li |
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Rok vydání: | 2020 |
Předmět: |
0301 basic medicine
Hepatitis B virus HBsAg Clinical Biochemistry Biology Virus Replication medicine.disease_cause Biochemistry 03 medical and health sciences Suppressor of Cytokine Signaling 1 Protein 0302 clinical medicine microRNA Autophagy medicine Humans Protein kinase B PI3K/AKT/mTOR pathway Hep G2 Cells Cell Biology General Medicine Transfection digestive system diseases Cell biology MicroRNAs 030104 developmental biology Viral replication 030220 oncology & carcinogenesis Signal Transduction |
Zdroj: | Cell Biochemistry and Function. 38:436-442 |
ISSN: | 1099-0844 0263-6484 |
Popis: | As small conserved RNAs without a coding function, microRNAs are expressed in multicellular organisms and contribute to the modulation of multiple cellular reactions, such as viral replication, as well as autophagy. microRNAs can regulate host gene expression and inhibit or reinforce hepatitis B virus (HBV) replication. Hepatic cells express miR-155 noticeably. Consequently, our study explored miR-155 modulation of HBV replication and investigated the potential mechanism involved. miR-155 was inhibited on HBV infection. miR-155 transfection remarkably reinforced HBV replication, antigen expression, and progeny secretion in HepG2215 cells. Moreover, miR-155 impaired the inhibition of the cytokine signalling 1 (SOCS1)/Akt/mTOR axis and reinforced HepG2215 autophagy. Additionally, the autophagy inhibitor (3-MA) eliminated HBsAg secretion triggered by miR-155. Taken together, miR-155 reinforced HBV replication by reinforcing SOCS1-triggered autophagy. SIGNIFICANCE OF THE STUDY: The research studied the potential mechanism involved in HBV replication and miR-155 that miR-155 reinforces HBV replication by reinforcing the SOCS1/Akt/mTOR axis-stimulated autophagy, and therefore, it can provide medical practitioners with the inspiration that chronic HBV might be cured or improved by regulating the activation of miR-155 in cells. In the study, the experiments show that autophagy inhibitors (3-MA) counteracted miR-155 contribution to HBV replication, and it might be a practicable way to improve HBV through some therapies that can repress the autophagy in related cells. |
Databáze: | OpenAIRE |
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