Oxidative stress and HPV carcinogenesis.
Oxidative stress and HPV carcinogenesis.
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DOI：
10.3390/v5020708
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发表时间：
2013-02-12
期刊：
影响因子：
--
通讯作者：
De Marco F
中科院分区：
文献类型：
--
作者：
De Marco F
广泛的实验工作已经最终证明，感染某些类型的人乳头瘤病毒，即所谓的高危人乳头瘤病毒（HR-HPV），是最强大的人类致癌物质。然而，在HPV的自然史中，肿瘤生长是一种罕见且不适当的结果，并且为了诱导病毒感染进入（非常罕见的）肿瘤转化，必须同时发生许多其他事件。从这个角度来看，一些假定的病毒，宿主和环境的辅因子已被提出作为潜在的候选人。其中氧化应激（OS）是一个有趣的候选人，但相对探索不足。OS是在线粒体氧化磷酸化期间以及在炎症、感染、电离辐射、UV暴露、机械和化学应力期间产生的对需氧生物体的持续威胁。上皮组织是HPV感染的选择性靶点，大量暴露于所有指定的OS来源。OS和HPV之间可能存在两种不同类型的合作机制：I）OS遗传毒性活性和HPV诱导的基因组不稳定性独立地与肿瘤克隆出现所必需的分子损伤的产生一致。该第一种模式仅仅是一种特定形式的共致癌作用;和II）OS与HPV感染诱导的肿瘤起始和/或进展的一个或多个分子阶段特异性相互作用。这份手稿旨在总结关于后一种假设的可用数据。本文将对OS在病毒感染和病毒整合过程中的实验数据和间接证据进行综述。NO（一氧化氮）和iNOS（诱导型一氧化氮合酶）的抗凋亡和促血管生成作用将与OS/HPV在诱导癌症代谢适应中的合作一起讨论。将强调OS与HPV驱动的致癌作用相互作用的未探索/未充分探索的方面。本文的目的是激发新的研究领域和创新方法。
Extensive experimental work has conclusively demonstrated that infection with certain types of human papillomaviruses, the so-called high-risk human papillomavirus (HR-HPV), represent a most powerful human carcinogen. However, neoplastic growth is a rare and inappropriate outcome in the natural history of HPV, and a number of other events have to concur in order to induce the viral infection into the (very rare) neoplastic transformation. From this perspective, a number of putative viral, host, and environmental co-factors have been proposed as potential candidates. Among them oxidative stress (OS) is an interesting candidate, yet comparatively underexplored. OS is a constant threat to aerobic organisms being generated during mitochondrial oxidative phosphorylation, as well as during inflammation, infections, ionizing irradiation, UV exposure, mechanical and chemical stresses. Epithelial tissues, the elective target for HPV infection, are heavily exposed to all named sources of OS. Two different types of cooperative mechanisms are presumed to occur between OS and HPV: I) The OS genotoxic activity and the HPV-induced genomic instability concur independently to the generation of the molecular damage necessary for the emergence of neoplastic clones. This first mode is merely a particular form of co-carcinogenesis; and II) OS specifically interacts with one or more molecular stages of neoplastic initiation and/or progression induced by the HPV infection. This manuscript was designed to summarize available data on this latter hypothesis. Experimental data and indirect evidences on promoting the activity of OS in viral infection and viral integration will be reviewed. The anti-apoptotic and pro-angiogenetic role of NO (nitric oxide) and iNOS (inducible nitric oxide synthase) will be discussed together with the OS/HPV cooperation in inducing cancer metabolism adaptation. Unexplored/underexplored aspects of the OS interplay with the HPV-driven carcinogenesis will be highlighted. The aim of this paper is to stimulate new areas of study and innovative approaches.
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影响因子：
3.7
作者：
De Marco F;Bucaj E;Foppoli C;Fiorini A;Blarzino C;Filipi K;Giorgi A;Schininà ME;Di Domenico F;Coccia R;Butterfield DA;Perluigi M
通讯作者：
Perluigi M
影响因子：
20.1
作者：
Al-Mehdi, AB;Zhao, GC;Fisher, AB
通讯作者：
Fisher, AB
影响因子：
--
作者：
Bartsch, H;Nair, J
通讯作者：
Nair, J
影响因子：
3.3
作者：
Cadet J;Loft S;Olinski R;Evans MD;Bialkowski K;Richard Wagner J;Dedon PC;Møller P;Greenberg MM;Cooke MS
通讯作者：
Cooke MS
DOI：
10.1073/pnas.96.11.6161
发表时间：
1999-05-25
影响因子：
11.1
作者：
Åslund, F;Zheng, M;Storz, G
通讯作者：
Storz, G