乙型肝炎病毒驱动甲胎蛋白表达诱导肝细胞恶性转化的分子机制  

Hepatitis B Virus-driven Expression of Alpha Fetoprotein-induced Malignant Liver Cell Transformation

作　　者：朱明月[1,2] 夏华[1,3] 李孟森[1,3] 

机构地区：[1]海南省肿瘤发生和干预重点实验室,海南医学院 [2]海南大学农学院,海南海口570228 [3]海南医学院分子生物学重点实验室,海南海口571199

出　　处：《中国生物化学与分子生物学报》2013年第9期814-819,共6页Chinese Journal of Biochemistry and Molecular Biology

基　　金：国家自然科学基金资助项目(No.81360307,81260306,81160261,31060164);教育部新世纪优秀人才支持计划(No.NCET-10-0124);教育部重点科技项目(No.211146);海南省重点科技项目(No.DZXM20110038);海南省自然科学基金资助项目(No.309034,310044)~~

摘　　要：肝癌细胞的恶性转化与感染乙型肝炎病毒(hepatitis B virus,HBV)和丙型肝炎病毒密切相关.但是HBV没有直接诱导肝癌发生的生物学功能,HBV可通过其x蛋白(HBx)激活生长信号,促进癌基因的表达从而诱导肝细胞恶性转化.在肝细胞恶性转化过程的早期,甲胎蛋白(alpha fetoprotein,AFP)基因被激活,而AFP能激发PI3K/AKT信号传递,由于PI3K/AKT信号途径具有促进细胞恶性转化的作用,所以AFP的表达在HBV诱导肝细胞恶性转化过程发挥关键性作用.本文就HBV通过优先驱动AFP表达促进肝癌细胞增殖和自然重编程从而诱发肝癌的分子机制进行阐述,对认识AFP在HBV相关性肝癌发生过程中的作用以及预警肝癌发生有重要的科学意义.Hepatocarcinogenesis is closely related with infection of hepatitis B and C viruses Hepatocellular carcinoma （HCC） does not directly induced by HBVs, nevertheless, the oncogene expression can be stimulated by the HBV x protein through cancer-related signals. The activation of oncogenes could lead to malignant transformation of liver ceils. Alpha fetoprotein （AFP） was up- regulated during the early stages of hepatoearcinogenesis, where the PI3K/AKT signal was triggered involving AFP as a critical factor. We explored the molecular mechanism of HBV regulated expression of AFP in the proliferation and reprogramming of liver cells during the malignant transformation of hepatocytes. This review will be helpful for understanding the role of AFP in the development of HCC, particularly for AFP as an earl,/ indicator during HBV-related hepatocarcinogenesis.

关 键 词：肝细胞恶性转化 乙型肝炎病毒 甲胎蛋白 

分 类 号：Q78[生物学—分子生物学]