中国麻风皮肤病杂志 ›› 2018, Vol. 34 ›› Issue (12): 749-754.

• 综述 • 上一篇    下一篇

人乳头瘤病毒致皮肤肿瘤机制的研究进展

朱宸朴, 黄 丹, 陈 崑   

  1. 中国医学科学院北京协和医学院皮肤病研究所理疗科,南京，210042
  • 出版日期:2018-12-13 发布日期:2018-12-14
  • 通讯作者: 陈崑，E-mail：kunchen181@aliyun.com

Update of HPV -induced skin neoplasm

ZHU Chenpu, HUANG Dan, CHEN Kun   

  1. Institute of Dermatology, Chinese Academy of Medical Sciences and Peking Union Medical College, Nanjing 210042, China
  • Online:2018-12-13 Published:2018-12-14
  • Contact: CHEN Kun, E-mail: kunchen181@aliyun.com

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摘要： 人乳头瘤病毒 (HPV)是一种环状双链DNA病毒，具有噬上皮特性，分为高危型和低危型两类，分别能导致上皮细胞的良性增生与恶变，E5、E6、E7蛋白，L1/L2衣壳蛋白参与高危型HPV引起上皮细胞恶性肿瘤的机制。E6蛋白可抑制PDZ蛋白、Daxx蛋白等抑癌蛋白的作用，激活端粒酶导致细胞永生化，E7蛋白主要通过引起多条信号通路紊乱、介导免疫逃逸、影响多种原癌基因的mi-RNA转录诱导上皮细胞恶变。而E5蛋白、L1/L2衣壳蛋白主要作用是增强E6与E7蛋白的致癌性。本文对人乳头瘤病毒致皮肤肿瘤机制研究进展进行综述。

关键词: 皮肤肿瘤, 人乳头瘤病毒, 机制

Abstract: Human papillomavirus (HPV) is a circular double-stranded DNA virus with phagocytic properties. HPV is classified as high-risk and low-risk types according to the pathogenicity, which can respectively lead to benign hyperplasia and malignant transformation of epithelial cells. E5, E6, E7 and L1 / L2 capsid proteins are generally involved in carcinogenesis and E6 may inhibit the function of PDZ and Daxx protein, E7 protein affect the transcription of a variety of mi-RNA through making the multiple signal pathways disorder and mediates immune escape. E5 protein and L1 / L2 capsid protein can enhance the carcinogenesi of E6 and E7 protein. The update mechanism of HPV -induced skin tumor is reviewed in this paper.

Key words: human papillomavirus, skin neoplasm；mechanism