人乳头瘤病毒致皮肤肿瘤机制的研究进展  

Update of HPV-induced skin neoplasm

作　　者：朱宸朴 黄丹[1] 陈崑[1] ZHU Chenpu;HUANG Dan;CHEN Kun(Institute of Dermatology,Chinese Academy of Medical Sciences and Peking Union Medical College,Nanjing 210042,China)

机构地区：[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　　处：《中国麻风皮肤病杂志》2018年第12期749-754,共6页China Journal of Leprosy and Skin Diseases

基　　金：江苏省自然科学基金(编号:BK20160152)

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。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.

关 键 词：皮肤肿瘤 人乳头瘤病毒 机制 

分 类 号：R739.5[医药卫生—肿瘤]