Role of melatonin in the epigenetic regulation of breast cancer

Ahmet Korkmaz, Emilio J. Sanchez-Barcelo, Dun Xian Tan, Russel J. Reiter

Research output: Contribution to journalReview articlepeer-review

59 Scopus citations

Abstract

The oncostatic properties of melatonin as they directly or indirectly involve epigenetic mechanisms of cancer are reviewed with a special focus on breast cancer. Five lines of evidence suggest that melatonin works via epigenetic processes: (1) melatonin influences transcriptional activity of nuclear receptors (ERα, GR and RAR) involved in the regulation of breast cancer cell growth; (2) melatonin down-regulates the expression of genes responsible for the local synthesis or activation of estrogens including aromatase, an effect which may be mediated by methylation of the CYP19 gene or deacetylation of CYP19 histones; (3) melatonin inhibits telomerase activity and expression induced by either natural estrogens or xenoestrogens; (4) melatonin modulates the cell cycle through the inhibition of cyclin D1 expression; (5) melatonin influences circadian rhythm disturbances dependent on alterations of the light/dark cycle (i.e., light at night) with the subsequent deregulation of PER2 which acts as a tumor suppressor gene.

Original languageEnglish (US)
Pages (from-to)13-27
Number of pages15
JournalBreast Cancer Research and Treatment
Volume115
Issue number1
DOIs
StatePublished - May 2009

Keywords

  • Aromatase
  • Breast cancer
  • Cell cycle
  • Clock genes
  • Epigenetic mechanisms
  • Light at night
  • Melatonin
  • Nuclear receptors
  • Telomerase

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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