Published online Oct 14, 2015. doi: 10.3748/wjg.v21.i38.10732
Peer-review started: May 6, 2015
First decision: June 2, 2015
Revised: June 24, 2015
Accepted: September 2, 2015
Article in press: September 2, 2015
Published online: October 14, 2015
Processing time: 169 Days and 2.3 Hours
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.
Core tip: The mechanisms underlying hepatitis B virus (HBV)-induced malignant transformation remain ambiguous, but research has suggested that HBV X (HBx) protein has a crucial function in the pathogenesis of hepatocellular carcinoma. This review focuses on the pathological functions of HBx in HBV-induced hepatocarcinogenesis.