Context-specific regulation of cancer epigenomes by histone and transcription factor methylation

Oncogene. 2014 Mar 6;33(10):1207-17. doi: 10.1038/onc.2013.87. Epub 2013 Mar 18.


Altered expression or activity of histone lysine methylases and demethylases in cancer lead to aberrant chromatin modification patterns, which contribute to uncontrolled cell proliferation via cancer-specific deregulation of gene expression programs or the induction of genome instability. Several transcription factors that regulate growth-associated genes undergo lysine methylation, expanding the repertoire of regulatory targets modulated by histone-methylating enzymes during tumorigenesis. In certain specific tumor types or specific physiological conditions, these enzymes may trigger chromatin structure and/or transcription factor activity changes that result in opposite effects on cancer initiation or progression. The mechanisms of such context-specific dual functions and those involved in the crosstalk between factor and histone modifications are subject to extensive research, which is beginning to shed light into this novel level of complexity of cancer-related epigenetic pathways.

Publication types

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

MeSH terms

  • Chromatin / metabolism
  • Epigenesis, Genetic*
  • Gene Expression Regulation, Neoplastic*
  • Histone-Lysine N-Methyltransferase / metabolism
  • Histones / metabolism
  • Humans
  • Methylation
  • Neoplasms / genetics*
  • Neoplasms / metabolism
  • Protein Processing, Post-Translational*
  • Transcription Factors / metabolism


  • Chromatin
  • Histones
  • Transcription Factors
  • Histone-Lysine N-Methyltransferase