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Hepatitis B virus X protein protects hepatoma and hepatic cells from complement‐dependent cytotoxicity by up‐regulation of CD46
Author(s) -
Zhang Shuai,
Shan Changliang,
Cui Wenjing,
You Xiaona,
Du Yumei,
Kong Guangyao,
Gao Fabao,
Ye Lihong,
Zhang Xiaodong
Publication year - 2013
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2013.01.019
Subject(s) - hbx , cd46 , creb , stat3 , cytotoxicity , hepatitis b virus , complement dependent cytotoxicity , chemistry , stat1 , microbiology and biotechnology , biology , signal transduction , transcription factor , cancer research , complement system , antibody , virus , antibody dependent cell mediated cytotoxicity , virology , in vitro , gene , immunology , biochemistry
The involvement of hepatitis B virus X protein (HBx) in anti‐complement‐dependent cytotoxicity (CDC) activity during hepatocarcinogenesis is poorly understood. Here, we report that HBx is able to up‐regulate membrane‐bound complement regulatory protein CD46 in hepatoma cells and human immortalized liver cells through activating the promoter activity involving cAMP response element‐binding protein (CREB)/cyclooxygenase‐2 (COX‐2)/prostaglandin E2 (PGE2)/signal transducers and activators of transcription 3 (STAT3) signaling pathway. In contrast, the down‐regulation of CD46 abolishes the resistance capability of hepatoma cells to CDC. Thus, we conclude that HBx contributes to the protection of hepatoma and hepatic cells from CDC by up‐regulation of CD46.