高危型人乳头瘤病毒癌基因E6和E7调节细胞作用靶点的研究进展  

Advances in the study of regulatory targets for high-risk human papillomavirus oncogenes E6 and E7

作　　者：刘淼[1] 孙峥嵘[1] LIU Miao;SUN Zhengrong(Biobank of Shengjing Hospital Affiliated to China Medical University,Liaoning Shenyang 110000,China)

机构地区：[1]中国医科大学附属盛京医院生物样本库,辽宁沈阳110000

出　　处：《现代肿瘤医学》2022年第4期748-752,共5页Journal of Modern Oncology

基　　金：辽宁省重点研发计划(编号:2018225009);辽宁省高等学校基本科研项目(编号:LFWK201710)。

摘　　要：高危型人乳头瘤病毒(human papillomavirus,HPV)的感染与多种人类癌症密切相关,其中最典型的是宫颈癌。高危型HPV最重要的两个病毒癌基因为E6和E7,病毒基因组整合到宿主基因组是病毒癌基因E6和E7实现持续表达的一种方式。HPV癌基因E6和E7能够靶向宿主细胞途径,通过这些相互作用,导致HPV发挥其在细胞中的致癌作用。对于病毒癌基因E6和E7研究最充分的细胞靶点分别是p53和pRb,然而,最近的研究表明这两种病毒蛋白具有调节更多细胞作用靶点的能力,包括细胞中调节表观遗传标记和剪接变化的蛋白质等。高危型HPV E6和E7蛋白通过调节这些靶点使细胞发生过度增殖和致癌作用。Infection of high-risk human papillomavirus(HPV)is closely related to a variety of human cancers,the most prominent of which is cervical cancer.The two most important viral oncogenes for high-risk HPV are E6 and E7,and the integration of the viral genome into the host genome is one of the manners in which the viral oncogenes E6 and E7 achieve persistent expression.HPV exerts its tumorigenicity in cells.The most well-studied cellular targets for viral oncogenes E6 and E7 are p53 and pRb,respectively.However,recent studies have shown that the ability of these two viral proteins to target more cellular factors,including proteins that regulate epigenetic markers and splicing changes in cells.HPV oncogenes E6 and E7 have the ability to exert a global change in cells through these interactions,which eventually culminates to uncontrolled proliferation and carcinogenesis.

关 键 词：高危型人乳头瘤病毒 E6 E7 细胞作用靶点 

分 类 号：R730[医药卫生—肿瘤]