Role of STAT1 in the resistance of HBV to IFN‑α

Xu, Baohua; Tang, Bo; Wei, Jiajia

doi:10.3892/etm.2021.9982

Cited by 5 publications

(2 citation statements)

References 36 publications

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“…Specifically, there was a marked decrease in the phosphorylation of STAT1 in the IFNαresistant HepG2.2.15 cells, concomitant with a down-regulation in the expression of the 2′,5′-oligoadenylate synthetase 1. These findings suggest that disruptions in the JAK-STAT pathway, particularly reduced STAT1 phosphorylation, could support IFN-α treatment resistance observed in HBV patients (Xu et al, 2021) (Figure 3).…”

Section: The Interaction Of Hbx and Ifn Signal Pathway Regulation Of ...mentioning

confidence: 75%

Role of hepatitis B virus non-structural protein HBx on HBV replication, interferon signaling, and hepatocarcinogenesis

Wang,

Song,

et al. 2023

Front. Microbiol.

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Hepatitis B, a global health concern caused by the hepatitis B virus (HBV), infects nearly 2 billion individuals worldwide, as reported by the World Health Organization (WHO). HBV, a hepatotropic DNA virus, predominantly targets and replicates within hepatocytes. Those carrying the virus are at increased risk of liver cirrhosis and hepatocellular carcinoma, resulting in nearly 900,000 fatalities annually. The HBV X protein (HBx), encoded by the virus’s open reading frame x, plays a key role in its virulence. This protein is integral to viral replication, immune modulation, and liver cancer progression. Despite its significance, the precise molecular mechanisms underlying HBx remain elusive. This review investigates the HBx protein’s roles in HBV replication, interferon signaling regulation, and hepatocellular carcinoma progression. By understanding the complex interactions between the virus and its host mediated by HBx, we aim to establish a solid foundation for future research and the development of HBx-targeted therapeutics.

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Section: The Interaction Of Hbx and Ifn Signal Pathway Regulation Of ...mentioning

confidence: 75%

Role of hepatitis B virus non-structural protein HBx on HBV replication, interferon signaling, and hepatocarcinogenesis

Wang,

Song,

et al. 2023

Front. Microbiol.

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“…A number of studies have reported that IFN-α-2b can activate STAT1, resulting in the phosphorylation of STAT1 [30,31]. STAT1 is a member of STAT protein family.…”

Section: Discussionmentioning

confidence: 99%

IFN-α-2b Reduces Postoperative Arthrofibrosis in Rats by Inhibiting Fibroblast Proliferation and Migration through STAT1/p21 Signaling Pathway

Liu

Fan

Wang

et al. 2023

Mediators of Inflammation

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Objective. To investigate the effect of IFN-α-2b in preventing postoperative arthrofibrosis in rats, its antiproliferation effect on fibroblasts in vitro, and its molecular mechanism. Methods. The rat model of arthrofibrosis was established and treated with different concentrations of drugs. Knee specimens were collected for histological and immunohistochemical staining to observe the effect of IFN-α-2b on arthrofibrosis in rats. The biological information was further mined according to the database data, and the possible regulatory mechanism of IFN-α-2b on fibroblasts was analyzed. The inhibitory effect of IFN-α-2b on fibroblast proliferation and migration in vitro was detected by cell counting kit-8 (CCK-8), immunofluorescence analysis, cell cycle test, EdU assay, wound healing test, and Transwell method, and the analysis results were verified by Western blotting method. Results. The test results of rat knee joint specimens showed that IFN-α-2b significantly inhibited the degree of fibrosis after knee joint surgery, the number of fibroblasts in the operation area was less than that of the control group, and the expression of collagen and proliferation-related proteins decreased. In vitro experimental results show that IFN-α-2b can inhibit the proliferation and migration of fibroblasts. According to the results of database analysis, it is suggested that the STAT1/P21 pathway may be involved, and it has been verified and confirmed by Western blotting and other related methods. Conclusion. IFN-α-2b can reduce surgery-induced arthrofibrosis by inhibiting fibroblast proliferation and migration, which may be related to the regulation of STAT1/p21 signaling pathway.

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STAT1 is associated with NK cell dysfunction by downregulating NKG2D transcription in chronic HBV-infected patients

Huang

Mo²,

Fu³

et al. 2022

Immunobiology

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Role of STAT1 in the resistance of HBV to IFN‑α

Cited by 5 publications

References 36 publications

Role of hepatitis B virus non-structural protein HBx on HBV replication, interferon signaling, and hepatocarcinogenesis

Role of hepatitis B virus non-structural protein HBx on HBV replication, interferon signaling, and hepatocarcinogenesis

IFN-α-2b Reduces Postoperative Arthrofibrosis in Rats by Inhibiting Fibroblast Proliferation and Migration through STAT1/p21 Signaling Pathway

STAT1 is associated with NK cell dysfunction by downregulating NKG2D transcription in chronic HBV-infected patients

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