
Hepatitis B virus X protein enhances NFκB activity through cooperating with VBP1
Author(s) -
Sang Yong Kim,
Jin Chul Kim,
Jeong Ki Kim,
Hye Jin Kim,
Hee Min Lee,
Mi Sun Choi,
Pil Jae Maeng,
Jeong Keun Ahn
Publication year - 2008
Publication title -
bmb reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.511
H-Index - 77
eISSN - 1976-670X
pISSN - 1976-6696
DOI - 10.5483/bmbrep.2008.41.2.158
Subject(s) - hbx , transactivation , immunoprecipitation , hepatitis b virus , carcinogenesis , hepatocellular carcinoma , biology , suppressor , cancer research , chemistry , virus , virology , transcription factor , cell culture , gene , genetics
Hepatitis B virus X protein (HBx) is essential for hepatitis B virus infection and exerts a pleiotropic effect on various cellular machineries. HBx has been also demonstrated as an indirect transcriptional transactivator of various different viral and cellular promoters. In addition, HBx is involved in the development of various liver diseases including hepatocellular carcinoma. However the mechanism of HBx in hepatocellular carcinogenesis remains largely unknown. In this study, to identify possible new cellular proteins interacting with HBx, we carried out yeast two-hybrid assay. We obtained several possible cellular partners including VBP1, a binding factor for VHL tumor suppressor protein. The direct physical interaction between HBx and VBP1 in vitro and in vivo was confirmed by immunoprecipitation assay. In addition, we found that VBP1 facilitates HBx-induced NFkappaB activation and cell proliferation. These results implicate the important role of HBx in the development of hepatocellular carcinoma through its interaction with VBP1.