蔡平平, 黄建炜, 苏成豪, 崔秀灵, 许瑞安. 乙肝病毒X蛋白与肝癌的关系J. 药学学报, 2016,51(2): 165-173. doi: 10.16438/j.0513-4870.2015-0570
引用本文: 蔡平平, 黄建炜, 苏成豪, 崔秀灵, 许瑞安. 乙肝病毒X蛋白与肝癌的关系J. 药学学报, 2016,51(2): 165-173. doi: 10.16438/j.0513-4870.2015-0570
CAI Ping-ping, HUANG Jian-wei, SU Cheng-hao, CUI Xiu-ling, XU Rui-an. Relationship between hepatitis B virus X protein and hepatic cellular cancerJ. Acta Pharmaceutica Sinica, 2016,51(2): 165-173. doi: 10.16438/j.0513-4870.2015-0570
Citation: CAI Ping-ping, HUANG Jian-wei, SU Cheng-hao, CUI Xiu-ling, XU Rui-an. Relationship between hepatitis B virus X protein and hepatic cellular cancerJ. Acta Pharmaceutica Sinica, 2016,51(2): 165-173. doi: 10.16438/j.0513-4870.2015-0570

乙肝病毒X蛋白与肝癌的关系

Relationship between hepatitis B virus X protein and hepatic cellular cancer

  • 摘要: 在全球范围内,肝细胞癌(hepatic cellular cancer, HCC)作为一类最普遍的癌症,严重影响着人们的身心健康和生命。平均每年有700000人死于肝癌,且发病率逐年增长。乙型肝炎病毒(hepatitis B virus, HBV)感染已经被认为是HCC发生的危险性影响因素。然而, HBV诱导的肝癌发生的发病机制尚未清楚。有证据显示, HBV X蛋白(hepatitis B virus X protein, HBx)在肝癌转化和恶性转移过程中扮演着关键角色。HBx是一个多功能的调节因子,与宿主相关因子协作,发挥其功能,能调节转录、信号转导通路、细胞周期进程、凋亡、蛋白降解途径、抑癌基因和原癌基因的表达。本文主要从分子机制方面阐述HBx诱导肝癌发生的最新研究成果。

     

    Abstract: Hepatic cellular cancer (HCC) is one of the most common cancers in the world, which is a serious threat to human health and life quality. More than 700 000 people die of HCC each year on average, and its incidence increases in many countries. Chronic hepatitis B virus (HBV) infection has been identified as a dominant risk factor for HCC. The pathogenesis of HBV-induced hepatocarcinogenesis is, however, incom-pletely understood. Evidence currently available supports a key role of the HBV X protein (HBx) in the cancer transformation and malignant tumor metastasis. HBx is a multifunctional regulator that may cooperate with the host factors to exert its effects on transcription, signal transduction, cell cycle progression, apoptosis, protein degradation, expression of oncogene and anti-oncogene. This review presents the current knowledge in the molecular pathogenesis of HBx in the induction of HCC.

     

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