Molecular mechanism of hepatitis B virus X protein function in hepatocarcinogenesis

被引:61
作者
Geng, Ming [1 ]
Xin, Xuan [1 ]
Bi, Li-Quan [1 ]
Zhou, Lu-Ting [1 ]
Liu, Xiao-Hong [1 ]
机构
[1] Jinan Mil Command, Gen Hosp, Dept Pathol, Shifang Rd 25, Jinan 250031, Shandong, Peoples R China
基金
美国国家科学基金会;
关键词
Hepatocellular carcinoma; Hepatitis B virus; Hepatitis B virus X protein; Hepatocarcinogenesis; NF-KAPPA-B; HEPATOCELLULAR-CARCINOMA; CORE PROMOTER; SIGNALING PATHWAY; UP-REGULATION; HBX MUTANTS; CELL-PROLIFERATION; NONCODING RNAS; LIVER-CELLS; MUTATIONS;
D O I
10.3748/wjg.v21.i38.10732
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
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-kappa B pathways. We conclude that HBx hastens the development of hepatoma.
引用
收藏
页码:10732 / 10738
页数:7
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