国际妇产科学杂志

国际妇产科学杂志 ›› 2011, Vol. 38 ›› Issue (2): 120-122.

• 综述 • 上一篇    下一篇

人乳头瘤病毒3种早期癌蛋白致癌作用的研究进展

张 栋 瞿全新   

  1. 300192 天津医科大学一中心临床学院妇科
  • 收稿日期:1900-01-01 修回日期:1900-01-01 出版日期:2011-04-15 发布日期:2011-04-15

Progress of Study on Carcinogenesis of Three HPV Early Oncoproteins

ZHANG Dong, QU Quan-xin   

  1. Department of Gynecology, the First Central Clinical College, Tianjin Medical University, Tianjin 300192, China
  • Received:1900-01-01 Revised:1900-01-01 Published:2011-04-15 Online:2011-04-15

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摘要： 高危型人乳头瘤病毒（HR-HPV）感染是导致宫颈癌的重要原因。E5，E6，E7是HR-HPV编码的3种早期癌蛋白，对宫颈上皮细胞有刺激生长和转化功能。近期研究发现，E5在癌症发生的早期阶段通过干预生长因子受体，干扰细胞周期蛋白和细胞周期蛋白依赖激酶（CDKs），促进病毒癌基因的转化等过程发挥致癌作用。E6干预P53，使其对细胞生长负调节功能丧失，失去对细胞周期的正常调控，引起细胞无限增生并向恶性转化。E7干预视网膜母细胞瘤（Rb）蛋白，解除其抑制细胞增殖功能，发挥致癌作用。综述这3种早期癌蛋白致癌机制的研究进展。

关键词: 宫颈肿瘤, DNA肿瘤病毒, 乳头状瘤病毒科, 肿瘤蛋白质类, 人乳头瘤病毒16, 人乳头瘤病毒18

Abstract: HR-HPV infection is one of the important reasons for cervical cancer. E5, E6 and E7 are three early oncoproteins ecoded from HR-HPV, they can stimulate growth and transformation of cervical epithelial cells. Recent researches revealed that E5 could cause cancer by means of interfering the growth factor receptors, disturbing cyclins and CDKs and promoting the transformation of virus oncogenes. E6 could intervene P53 to lose its negatively adjustment function to cell proliferation, and cause cells proliferation and malignant transformation toward infinity. E7 could cause cancer mainly through intervention to remove the retinoblastoma cell proliferation function. This article is to review research progresses of carcinogenesis mechanism about the three oncoproteins.

Key words: Uterine cervical neoplasms, DNA tumor viruses, Papillomaviridae, Neoplasm proteins, Human papillomavirus 16, Human papillomavirus 18