Molecular mechanism of hepatitis B virus X protein function in hepatocarcinogenesis
Molecular mechanism of hepatitis B virus X protein function in hepatocarcinogenesis
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DOI：
10.3748/wjg.v21.i38.10732
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发表时间：
2015-10-14
影响因子：
4.3
通讯作者：
Liu, Xiao-Hong
中科院分区：
文献类型：
--
作者：
Geng, Ming;Xin, Xuan;Liu, Xiao-Hong
导致乙肝病毒相关性肝细胞癌的因素很多，包括乙肝病毒的产物、乙肝病毒的整合和变异以及宿主的易感性。HBx蛋白(HBx)可干扰多种与细胞增殖和侵袭相关的信号通路，HBx C端截短被认为影响了肝细胞癌的发生发展。现就HBx在乙肝病毒诱导的肝癌发生中的病理作用作一综述。作为一种反式激活因子，HBX可以影响调控的非编码RNA(NcRNAs)，包括microRNAs和长ncRNAs。HBx还参与表观遗传修饰和DNA修复。HBx与多种信号转导通路相互作用，如P53、Wnt和核因子-kappa B通路。我们的结论是，HBx加速了肝癌的发展。
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.