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Hepatitis B virus X protein promotes epithelial-mesenchymal transition of hepatocellular carcinoma cells by regulating SOCS1
Inho Kang1 (Graduate student), Ji Ae Kim1 (Research worker), Jin-chul Kim1 (Research worker), Ju Hyeon Lee1 (Graduate student), Mi-jee Kim1 (Graduate student), Jeong Keun Ahn 1,* (Professor)
1Department of Microbiology & Molecular Biology, College of Bioscience and Biotechnology, Chungnam National University
Hepatocellular carcinoma (HCC), a primary type of liver cancer, has one of the highest mortality rates in cancer related death worldwide. HCC patients have poor prognosis due to intrahepatic and extrahepatic metastasis. Hepatitis B virus (HBV) infection is one of the major causes of various liver diseases including HCC. Among HBV gene products, HBV X protein (HBx) plays important roles in the development and metastasis of HCC. However, the mechanisms of HCC metastasis induced by HBx has not been elucidated yet.
In this study, we first report that HBx interacts with regulates suppressor of cytokine signaling 1 (SOCS1) which negatively controls NF-リB by degrading p65, a subunit of NF-リB. NF-リB activates the transcription of factors associated with epithelial-mesenchymal transition (EMT) which is a crucial cellular process associated with invasiveness and migration of cancer cells. Here, we report that HBx physically binds to SOCS1, subsequently prevents the ubiquitination of p65, activates the transcription of EMT transcription factors, and enhances cell migration and invasiveness suggesting a new mechanism of HBV-associated HCC metastasis.
Abstract, Accepted Manuscript(in press) [Submitted on November 1, 2021, Accepted on December 26, 2021]
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