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- W4386593009 abstract "Cell apoptosis is strongly associated with hepatocellular carcinoma (HCC) progress. Thus, gaining a comprehensive understanding of the virus interfering with the apoptotic process is important for the development of effective anti-tumor therapies. The objective of this study is to explore the potential involvement of HBeAg-p22 (HBV-p22) in TNFα-induced apoptosis.Protein expression was detected using western blot. Cell viability and apoptosis were assessed by employing Cell Counting Kit-8 (CCK8) and flow cytometry, respectively. Evaluation of protein-protein interactions was accomplished through co-immunoprecipitation and glutathione-S-transferase (GST) pull-down assays.In this study, it was shown that HBV-p22 inhibited apoptosis of human hepatoma cell lines after tumor necrosis factor-alpha (TNF-α) stimulation. Mechanistically, HBV-p22 suppressed Jun N-terminal kinases (JNK) signaling and enhanced nuclear factor kappa-B (NF-κB) signaling. Moreover, HBV-p22 interacted with I-kappa B kinase α (IKKα) and increased its phosphorylation.Collectively, HBV-p22, whereby the mechanism contributing to anti-apoptotic effect was regulation of the NF-κB pathway via enhancing the phosphorylation of IKKα." @default.
- W4386593009 created "2023-09-12" @default.
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- W4386593009 date "2023-01-01" @default.
- W4386593009 modified "2023-10-02" @default.
- W4386593009 title "The hepatitis B virus pre-core protein p22 suppresses TNFα-induced apoptosis by regulating the NF-κB pathway." @default.
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