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作 者:蔡平平[1] 黄建炜[2] 苏成豪[2] 崔秀灵[1] 许瑞安[1]
机构地区:[1]华侨大学生物医学学院华侨大学分子药物研究院厦门市海洋与基因工程药物重点实验室,福建厦门361021 [2]华侨大学生物医学学院华侨大学分子药物研究院厦门市疾病预防与控制中心,福建厦门361021
出 处:《药学学报》2016年第2期165-173,共9页Acta Pharmaceutica Sinica
基 金:厦门市科技计划项目(3502Z2014015);厦门南方海洋研究中心(13GYY003NF16)
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700 000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。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, incompletely 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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