Redox control of viral carcinogenesis: The human papillomavirus paradigm.

摘要: Abstract Background Cervical cancer is the second most common neoplastic disease among women worldwide. The initiating event of such infection with certain types human papillomavirus (HPV), a very condition in general population. However, majority HPV infections subclinical and transitory resolved spontaneously. Intriguingly, viral oncogene expression, although necessary, not per se sufficient to promote cervical other factors are involved progression infected cells full phenotype. In this perspective it has been suggested that redox balance oxidative stress (OS) may represent interesting under-explored candidates as promoting HPV-initiated carcinogenesis. Scope review current discusses possible interplay between mechanisms modulating cell homeostasis sensitive mechanisms. Experimental data indirect evidences presented on activity dependent functions i) regulation enzymes compounds OS; ii) protection from oxidation detoxifying/antiapoptotic redox-sensitive transcription factors; iii) suppression apoptosis; iv) modulation host microRNAs regulating genes associated antioxidant defense. Major conclusions resulting tangled scenario suggests hosting adapt their metabolisms order support growth survival increasingly oxidant micro-environment tumor initiation progression. General significance can modulate favor possibly transformation. This article part Special Issue entitled Redox differentiation de-differentiation.