中国科技核心期刊
CN:31-1600/Q
ISSN:1004-0374
“健康与疾病的免疫”国际学术研讨会通知      关于有网站冒充本刊网站的声明
《生命科学》 2008, 20(2): 295-
人乳头瘤病毒(HPV)致癌机制研究进展
刘立鸿1,汪 凯2,张富春1,马正海1*
(1新疆大学生命科学与技术学院分子生物学重点实验室,新疆生物资源基因工程重点实验室, 乌鲁木齐 830046;2 中国科学院上海巴斯德研究所,上海 200025)
摘 要:人乳头瘤病毒(Human Papillomavirus,HPV)在人群中广泛传播,能引起皮肤和黏膜的异常增生,某些型的感染与生殖道恶性病变关系密切。HPV在致癌过程中,E2基因通常整合到宿主细胞基因组内,E2基因的失活和E5基因对EGFR的干预都能引起E6、E7基因过表达,E6、E7蛋白分别通过抑制p53、pRb基因的活性,从而激活人细胞端粒酶基因(hTERT)的转录,引起细胞分化异常,导致正常细胞癌化。HPV致癌是一个多因素、多步骤的渐进过程,其中协同因素也发挥重要作用。随着研究的深入,HPV的致癌机制越来越受到国内外研究者的重视,对HPV致癌机制的探索也逐渐成为研究热点。
关键词:人乳头瘤病毒;致癌机制;协同因素
中图分类号:R373; R730.231.3  文献标识码:A
 
Advances of research on the carcinogenesis of human Papillomavirus
LIU Li-hong1, WANG Kai2, ZHANG Fu-chun1, MA Zheng-hai1*
(1 Key Laboratory of Molecular Biology, Key Laboratory of Xinjiang Biological Resources and Genetic Engineering , College of Life Science and Technology, Xinjiang University,Urumqi 830046, China; 2 Institute Pasteur of Shanghai,Chinese Academy of Sc
Abstract: Human Papillomavirus(HPV) can be transmitted widely in human, which can cause human being{$39}s skin and mucosa of dysplasia. Some types of HPV are closely related with malignant genitalia disease. In the carcinogenic process of HPV, E2 gene normally integrates into the host cells, and resultes in the inactivation of E2 protein, which caused the over-expression of E6, E7 genes. Meanwhile, E5 gene sitimulates cell cycles via EGFR, which in turn raising the over-expression of E6, E7 genes. The activities of p53 gene and pRb gene are inhibited by HPV16 E6 and E7 proteins respectively, resulting in the activation of the transcription of hTERT, and the inblance of cells, which could change the cells from the normal to the cancer. The carcinogenic process of HPV is a multi-factor and multi-step process, in which genetic and synergistic factors also play an important role. With the in-depth study, the carcinogenic mechanism of HPV has been drawn increased attention of the basic researchers and clinicians. The explorations of the carcinogenic mechanism of HPV has become the hotspot in the research.
Key words: human Papillomavirus; carcinogenesis; synergistic factors
 
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