Present address: Genome Biology Unit, European Molecular Biology Laboratory, Heidelberg, Germany.
Insights & Perspectives
DNA methylation reprogramming in cancer: Does it act by re-configuring the binding landscape of Polycomb repressive complexes?
Version of Record online: 26 NOV 2013
© 2014 The Authors. Bioessays published by WILEY Periodicals, Inc.
This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
Volume 36, Issue 2, pages 134–140, February 2014
How to Cite
Reddington, J. P., Sproul, D. and Meehan, R. R. (2014), DNA methylation reprogramming in cancer: Does it act by re-configuring the binding landscape of Polycomb repressive complexes?. Bioessays, 36: 134–140. doi: 10.1002/bies.201300130
- Issue online: 14 JAN 2014
- Version of Record online: 26 NOV 2013
- Medical Research Council, IMI-MARCAR and the BBSRC
- University of Edinburgh and Breast Cancer Campaign
- cancer epigenetics;
- DNA methylation;
DNA methylation is a repressive epigenetic mark vital for normal development. Recent studies have uncovered an unexpected role for the DNA methylome in ensuring the correct targeting of the Polycomb repressive complexes throughout the genome. Here, we discuss the implications of these findings for cancer, where DNA methylation patterns are widely reprogrammed. We speculate that cancer-associated reprogramming of the DNA methylome leads to an altered Polycomb binding landscape, influencing gene expression by multiple modes. As the Polycomb system is responsible for the regulation of genes with key roles in cell fate decisions and cell cycle regulation, DNA methylation induced Polycomb mis-targeting could directly drive carcinogenesis and disease progression.
Editor's suggested further reading in BioEssays Unmasking risk loci: DNA methylation illuminates the biology of cancer predisposition Abstract