Proteomics analysis of protein expression and specific protein oxidation in human papillomavirus transformed keratinocytes upon UVB irradiation

Marzia Perluigi, Alessandra Giorgi, Carla Blarzino, Federico De Marco, Cesira Foppoli, Fabio Di Domenico, D. Allan Butterfield, M. Eugenia Schininà, Chiara Cini, Raffaella Coccia

Research output: Contribution to journalArticlepeer-review

23 Scopus citations


Increasing evidence supports the role of oxidative stress in cancer development. Ultraviolet (UV) irradiation is one of the major sources of oxidative stress through the generation of reactive oxygen species (ROS). Besides the physiological function of ROS in cellular homeostasis, accumulating reports suggest that ROS are involved in all stages of multistep cancer development. In order to investigate the involvement of oxidative damage into the mechanisms of tumour progression, we used a parallel proteomic approach to analyse the protein expression profile and to identify oxidatively modified proteins in human papillomavirus (HPV)-transformed keratinocytes (HK-168 cells) upon ultraviolet B (UVB) exposure. The HK-168 cells were obtained from normal human epidermal keratinocytes transfected with the whole genome of the high-risk HPV type 16, unanimously recognized as an etiological agent of cervical carcinoma. Because of its year-long latency, this tumour offers a convenient model to study the role of environmental concurring agents in the multistep malignant progression. By the protein expression profile, we identified 21 proteins that showed different expression levels in HK-168 cells treated with UVB in comparison with untreated cells. Focusing on the oxidative modifications occurring at the protein level, we identified five proteins that showed elevated protein carbonyls levels: α-enolase, heat shock protein 75, annexin 2, elongation factor Tu and elongation factor γ. Our results indicate that UVB-induced oxidative stress perturbs the normal redox balance and shifts HPV-transformed keratinocytes into a state in which the carbonylation of specific proteins is systematically induced. We suggest that UVB-induced modulation of protein expression combined with oxidative modification lead to protein dysfunction that might contribute to the malignant progression of transformed cells.

Original languageEnglish
Pages (from-to)1809-1822
Number of pages14
JournalJournal of Cellular and Molecular Medicine
Issue number8 B
StatePublished - Aug 2009


  • Cervical carcinoma
  • HPV
  • Oxidative stress
  • Proteomics

ASJC Scopus subject areas

  • Molecular Medicine
  • Cell Biology


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