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Role of STAT1 in the resistance of HBV to IFN-α
Bingfa Xu 1 , Bo Tang 2 , Jiajia Wei 3
Affiliations
Affiliations
1
Department of Pharmacy, The Third Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230061, P.R. China.
2
Department of Pharmacy, Huainan First People's Hospital, Huainan, Anhui 232007, P.R. China.
3
Department of Pharmacy, The First People's Hospital of Changzhou, Changzhou, Jiangsu 213000, P.R. China.
PMID: 33850522 PMCID: PMC8027746 DOI: 10.3892/etm.2021.9982
Free PMC article
Abstract
The objective of the present study was to explore the mechanism of hepatitis B virus (HBV) resistance to interferon (IFN), and the role of signal transducer and activator of transcription 1 (STAT1). HepG2.2.15 cells were stimulated with a long-term (6-24 weeks) low-dose interferon (IFN)α-2b (10-70 IU/ml), so as to construct and screen a HepG2.2.15 cell model resistant to IFNα-2b. The changes of STAT1 and other proteins in the JAK-STAT signaling pathway, before and after drug resistance, were compared. The phosphorylation of STAT1 in HepG2.2.15 cells resistant to IFNα-2b was significantly decreased, and the expression level of 2',5'-oligoadenylate synthetase 1 was downregulated. Decreased phosphorylation of STAT1 in the JAK-STAT signaling pathway a contributor to the development of resistance to IFN-α in HBV.
Keywords: Hepatitis B virus; drug resistance; interferon α-2b; phosphorylation; signal transducer and activator of transcription 1.
Copyright: © Xu et al. |
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发表于 2021-4-17 03:45