Epigenetic activation of immune genes in cervical cancer

Immunol Lett. 2014 Dec;162(2 Pt B):256-7. doi: 10.1016/j.imlet.2014.09.019. Epub 2014 Oct 13.

Abstract

Immune system provides us protection from infectious pathogens and tumors formation during lifetime. Cervical cancer (CC), and its cause, human papillomavirus (HPV) are both challenges for the immune system. We present here evidence of epigenetic activation of immune system genes in CC. Illumina Infinium Human Methylation 450K BeadChip identified genes, which were all significantly hypomethylated in CC tissue versus normal tissue. The GeneMANIA computer program identified a tight network between those genes. The most strongly correlated genes based on their function are immune effectors' process (AIM2, BST2, BTN3A3, and IL12RB1) and response to virus related genes (AIM2, BST2, and IL12RB1). Thus, activation of those genes through demethylation is probably triggered by HPV oncogenes. In conclusion, the immune system of women who do not develop CC is probably activated earlier through DNA demethylation.

Publication types

  • Letter
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Epigenesis, Genetic / immunology*
  • Female
  • Gene Expression Regulation, Neoplastic / immunology*
  • Genes, Neoplasm / immunology*
  • Humans
  • Uterine Cervical Neoplasms / immunology*
  • Uterine Cervical Neoplasms / pathology