Lou Zhifeng, Wang Sheng
Department of Dentistry, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, People's Republic of China.
J Int Med Res. 2014 Apr;42(2):247-60. doi: 10.1177/0300060513506655. Epub 2014 Jan 20.
Human papillomavirus (HPV) infection is clinically very common. It is usually a major risk factor in the development of cutaneous benign lesions, cervical cancer and a variety of other malignancies. The biological function of ubiquitination as an intracellular proteasomal-mediated form of protein degradation and an important modulator in the regulation of many fundamental cellular processes has been increasingly recognized over the last decade. HPV proteins have been demonstrated to evolve different strategies to utilize the ubiquitin system for their own purposes. The putative roles of E3 ubiquitin ligases in HPV-induced carcinogenesis have become increasingly apparent, although the mechanisms remain unclear. In this review we provide an update on the mechanisms of the involvement of E3 ubiquitin ligases in HPV-induced carcinogenesis, focusing on their interaction with HPV proteins and their roles in several signalling pathways. Targeting the E3 ubiquitin ligases might offer potential therapeutic strategies for HPV-related diseases in future.
人乳头瘤病毒（HPV）感染在临床上非常常见。它通常是皮肤良性病变、宫颈癌和多种其他恶性肿瘤发生发展的主要危险因素。在过去十年中，泛素化作为一种细胞内蛋白酶体介导的蛋白质降解形式以及许多基本细胞过程调控中的重要调节因子，其生物学功能越来越受到认可。已证明HPV蛋白会采用不同策略来利用泛素系统以实现自身目的。尽管机制尚不清楚，但E3泛素连接酶在HPV诱导的致癌作用中的假定作用已越来越明显。在本综述中，我们提供了关于E3泛素连接酶参与HPV诱导致癌作用机制的最新进展，重点关注它们与HPV蛋白的相互作用以及在几种信号通路中的作用。靶向E3泛素连接酶可能为未来HPV相关疾病提供潜在的治疗策略。
