Open AccessMolecular mechanism of hepatitis B virus X protein function in hepatocarcinogenesis
Author(s) -
Meiyu Geng,
Xuan Xin,
Liquan Bi,
Luting Zhou,
Xiaohong Liu
Publication year - 2015
Publication title -
world journal of gastroenterology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.427
H-Index - 155
eISSN - 2219-2840
pISSN - 1007-9327
DOI - 10.3748/wjg.v21.i38.10732
Subject(s) - hbx , hepatitis b virus , cccdna , transactivation , microrna , biology , signal transduction , cancer research , hepatocellular carcinoma , virology , virus , gene , microbiology and biotechnology , transcription factor , genetics , hbsag
Many factors are considered to contribute to hepatitis B virus (HBV)-associated hepatocellular carcinoma (HCC), including products of HBV, HBV integration and mutation, and host susceptibility. HBV X protein (HBx) can interfere with several signaling pathways associated with cell proliferation and invasion, and HBx C-terminal truncation has been suggested to impact the development of HCC. This review focuses on the pathological functions of HBx in HBV-induced hepatocarcinogenesis. As a transactivator, HBx can affect regulatory non-coding RNAs (ncRNAs), including microRNAs and long ncRNAs. HBx is also involved in epigenetic modification and DNA repair. HBx interacts with various signal-transduction pathways, such as the p53, Wnt, and nuclear factor-κB pathways. We conclude that HBx hastens the development of hepatoma.