Redox control of viral carcinogenesis: The human papillomavirus paradigm

Cesira Foppoli, Federico De Marco, Chiara Cini, M. Perluigi

Research output: Contribution to journalArticle

11 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)1622-1632
Number of pages11
JournalBBA - General Subjects
Volume1850
Issue number8
DOIs
Publication statusPublished - Aug 7 2014

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Oxidation-Reduction
Carcinogenesis
Oxidative stress
Uterine Cervical Neoplasms
Tumors
Oxidative Stress
Homeostasis
Neoplasms
Papillomavirus Infections
Enzymes
Infection
MicroRNAs
Oncogenes
Oxidants
Metabolism
Transcription Factors
Antioxidants
Genes
Modulation
Apoptosis

Keywords

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

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

Cite this

Redox control of viral carcinogenesis : The human papillomavirus paradigm. / Foppoli, Cesira; De Marco, Federico; Cini, Chiara; Perluigi, M.

In: BBA - General Subjects, Vol. 1850, No. 8, 07.08.2014, p. 1622-1632.

Research output: Contribution to journalArticle

Foppoli, Cesira ; De Marco, Federico ; Cini, Chiara ; Perluigi, M. / Redox control of viral carcinogenesis : The human papillomavirus paradigm. In: BBA - General Subjects. 2014 ; Vol. 1850, No. 8. pp. 1622-1632.
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AB - 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.

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