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Hepatitis B virus X protein enhances liver cancer cell migration by regulating calmodulin-associated actin polymerization
Mi-jee Kim1 (Graduate student), Jinchul Kim1 (Research scientist), Jin-su Im1 (Research scientist), Inho Kang1 (Graduate student), Jeong Keun Ahn 1,* (Professor)
1Microbiology & Molecular Biology, Chungnam National University
Abstract
Hepatitis B virus (HBV) infection is one of the major causes of hepatocellular carcinoma (HCC), which is a highly aggressive cancer. HBV X protein (HBx), one of four HBV gene products, plays pivotal roles in the development and metastasis of HCC. It has been reported that HBx induces liver cancer cell migration and reorganizes actin cytoskeleton, however the molecular basis for actin cytoskeleton reorganization remains obscure.
In the present study, we for the first time report that HBx promotes actin polymerization and liver cancer cell migration by regulating calcium modulated protein, calmodulin (CaM). HBx physically interacts with CaM to control the level of phosphorylated cofilin, an actin depolymerizing factor. Mechanistically, HBx interacts with CaM, liberates Hsp90 from its inhibitory partner CaM, enhances the activity of Hsp90, resulting in the activation of LIMK1/cofilin pathway. Interestingly, the interaction between HBx and CaM is calcium-dependent and requires CaM binding motif on HBx. These results indicate that HBx modulates CaM which plays a regulatory role in Hsp90/LIMK1/cofilin pathway of actin reorganization, suggesting a new mechanism of HBV-induced HCC metastasis specifically derived by HBx.
Abstract, Accepted Manuscript(in press) [Submitted on June 30, 2021, Accepted on August 6, 2021]
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