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Biochim Biophys Acta. 2015 Aug;1850(8):1622-32. doi: 10.1016/j.bbagen.2014.12.016. Epub 2014 Dec 19.

Redox control of viral carcinogenesis: The human papillomavirus paradigm.

Author information

1
Institute of Molecular Biology and Pathology, National Research Council, Rome, Italy.
2
Laboratory of Virology, Regina Elena National Cancer Institute, Rome, Italy.
3
Department of Biochemical Sciences, Sapienza University of Rome, Rome, Italy.
4
Department of Biochemical Sciences, Sapienza University of Rome, Rome, Italy. Electronic address: marzia.perluigi@uniroma1.it.

Abstract

BACKGROUND:

Cervical cancer is the second most common neoplastic disease among women worldwide. The initiating event of such cancer is the infection with certain types of human papillomavirus (HPV), a very common condition in the general population. However, the majority of HPV infections is subclinical and transitory and is resolved spontaneously. Intriguingly, viral oncogene expression, although necessary, is not per se sufficient to promote cervical cancer and other factors are involved in the progression of infected cells to the full neoplastic phenotype. In this perspective it has been suggested that the redox balance and the oxidative stress (OS) may represent interesting and under-explored candidates as promoting factors in HPV-initiated carcinogenesis.

SCOPE OF THE REVIEW:

The current review discusses the possible interplay between the viral mechanisms modulating cell homeostasis and redox sensitive mechanisms. Experimental data and indirect evidences are presented on the activity of viral dependent functions on i) the regulation of enzymes and compounds involved in OS; ii) the protection from oxidation of detoxifying/antiapoptotic enzymes and redox-sensitive transcription factors; iii) the suppression of apoptosis; and iv) the modulation of host microRNAs regulating genes associated with antioxidant defense.

MAJOR CONCLUSIONS:

The resulting tangled scenario suggests that viral hosting cells adapt their metabolisms in order to support their growth and survival in the increasingly oxidant micro-environment associated with HPV tumor initiation and progression.

GENERAL SIGNIFICANCE:

HPV can modulate the host cell redox homeostasis in order to favor infection and possibly tumor transformation. This article is part of a Special Issue entitled Redox regulation of differentiation and de-differentiation.

KEYWORDS:

Antioxidant systems; Cervical cancer; Human papillomavirus; Oxidative stress; Transcription factors

PMID:
25534611
DOI:
10.1016/j.bbagen.2014.12.016
[Indexed for MEDLINE]

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