人乳头瘤病毒16型（HPV-16）是众所周知的子宫颈癌和口咽癌的病因。E2蛋白，HPV-16中早期转录基因的产物被认为通过p53依赖性和p53非依赖性途径导致癌细胞死亡。本系统综述的主要目的是研究HPV16-E2蛋白作为凋亡诱导剂。彻底搜索MEDLINE/PubMed,科学直接，Scopus,和EBSCOhost数据库进行了HPV和凋亡或涉及HPV16-E2的细胞死亡的相关研究。搜索确定了967种出版物。1997年1月1日至2022年2月16日的11条记录符合纳入标准，符合数据提取和纳入条件。所有研究得出结论,HPV16-E2能够诱导转染细胞中的细胞死亡。来自高风险HPV-16的E2蛋白能够根据表达基因的位置通过不同的凋亡途径诱导凋亡。然而,机制尚不清楚，和进一步的研究是必要的。
Human papillomavirus type 16 (HPV-16) is a well-known etiological factor for cervical and oropharyngeal cancers. The E2 protein, the product of an early-transcribed gene in HPV-16, is postulated to cause the death of cancerous cells via p53-dependent and p53-independent pathways. The main aim of the present systematic
review was to study the HPV 16-E2 protein as an apoptosis-inducer agent. A thorough search of MEDLINE/PubMed, Science Direct, Scopus, and EBSCOhost databases was conducted for relevant studies on HPV AND apoptosis OR cell death where HPV 16-E2 was involved. The search identified 967 publications. Eleven records dated from 1 January 1997 to 16 February 2022 were found to meet the inclusion criteria and were eligible for data extraction and inclusion. All studies concluded that HPV 16-E2 was able to induce cell death in transfected cells. E2 proteins from the high-risk HPV-16 were able to induce apoptosis through different apoptotic pathways depending on the location of the expressed gene. However, the mechanism was still unclear, and further studies are warranted.
