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Int. J. Mol. Sci. 2017, 18(3), 586; doi:10.3390/ijms18030586

Hepatitis B Virus X Protein Stimulates Proliferation, Wound Closure and Inhibits Apoptosis of HuH-7 Cells via CDC42

1,* , 2,* and 1,3,4,*
State Key Laboratory of Proteomics, Beijing Proteome Research Centre, National Engineering Research Centre for Protein Drugs, National Centre for Protein Sciences Beijing, Institute of Radiation Medicine, Beijing 102206, China
State Key Laboratory for Conservation and Utilization of Subtropical Agro-Bioresources, Guangxi University, Nanning 530005, China
Key Laboratory of Combinatorial Biosynthesis and Drug Discoveryof Ministry of Education, School of Pharmaceutical Sciences, School of Basic Medical Science, Wuhan University, Wuhan 430071, China
Graduate School, Anhui Medical University, Hefei 230032, China
Authors to whom correspondence should be addressed.
Academic Editor: Akihiro Tamori
Received: 23 January 2017 / Revised: 16 February 2017 / Accepted: 4 March 2017 / Published: 8 March 2017
(This article belongs to the Section Molecular Pathology, Diagnostics, and Therapeutics)
View Full-Text   |   Download PDF [4020 KB, uploaded 8 March 2017]   |  


Chronic hepatitis B virus (HBV) infection has been considered as the major cause of hepatocellular carcinoma (HCC). Hepatitis B virus X protein (HBx) has been reported to be oncogenic. The underlying mechanisms of HBV-related HCC are not fully understood, and the role played by the HBx protein in HBV induced carcinogenesis remains controversial. CDC42, a member of the Rho GTPase family, has been reported to be overexpressed in several different cancers, including HBV-related HCC. However, the specific role of CDC42 in HCC development remains unclear. Here, we investigated the cellular mechanisms by which CDC42 was responsible for the higher proliferation of HuH-7 cells mediated by HBx. We found that the expression level of CDC42 and its activity were significantly increased in HuH-7-HBx cells. The deficiency of CDC42 using the CRISPR/Cas9 system and inhibition by specific inhibitor CASIN led to the reduction of HBx-mediated proliferation. Furthermore, we observed that IQ Motif Containing GTPase Activating Protein 1 (IQGAP1), the downstream mediator of the CDC42 pathway, might be involved in the carcinogenesis induced by HBx. Therefore, the HBx/CDC42/IQGAP1 signaling pathway may potentially play an important role in HBx-mediated carcinogenesis. View Full-Text
Keywords: HBx; CDC42; HuH-7 cell; quantitative proteomics; hepatocellular carcinoma HBx; CDC42; HuH-7 cell; quantitative proteomics; hepatocellular carcinoma

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Xu, Y.; Qi, Y.; Luo, J.; Yang, J.; Xie, Q.; Deng, C.; Su, N.; Wei, W.; Shi, D.; Xu, F.; Li, X.; Xu, P. Hepatitis B Virus X Protein Stimulates Proliferation, Wound Closure and Inhibits Apoptosis of HuH-7 Cells via CDC42. Int. J. Mol. Sci. 2017, 18, 586.

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