H3K27 Methylation: A Focal Point of Epigenetic Deregulation in Cancer

J. N. Nichol, D. Dupéré-Richer, T. Ezponda, J. D. Licht, W. H. Miller

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

47 Scopus citations

Abstract

Epigenetics, the modification of chromatin without changing the DNA sequence itself, determines whether a gene is expressed, and how much of a gene is expressed. Methylation of lysine 27 on histone 3 (H3K27me), a modification usually associated with gene repression, has established roles in regulating the expression of genes involved in lineage commitment and differentiation. Not surprisingly, alterations in the homeostasis of this critical mark have emerged as a recurrent theme in the pathogenesis of many cancers. Perturbations in the distribution or levels of H3K27me occur due to deregulation at all levels of the process, either by mutation in the histone itself, or changes in the activity of the writers, erasers, or readers of this mark. Additionally, as no single histone mark alone determines the overall transcriptional readiness of a chromatin region, deregulation of other chromatin marks can also have dramatic consequences. Finally, the significance of mutations altering H3K27me is highlighted by the poor clinical outcome of patients whose tumors harbor such lesions. Current therapeutic approaches targeting aberrant H3K27 methylation remain to be proven useful in the clinic. Understanding the biological consequences and gene expression pathways affected by aberrant H3K27 methylation may lead to identification of new therapeutic targets and strategies.

Original languageEnglish
Title of host publicationAdvances in Cancer Research, 2016
EditorsKenneth D. Tew, Paul B. Fisher, Paul B. Fisher
PublisherAcademic Press Inc.
Pages59-95
Number of pages37
ISBN (Print)9780128047880
DOIs
StatePublished - 2016
Externally publishedYes

Publication series

NameAdvances in Cancer Research
Volume131
ISSN (Print)0065-230X
ISSN (Electronic)2162-5557

Keywords

  • Cancer
  • EZH2
  • Epigenetics
  • H3K27 methylation
  • PRC2

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