DNA methylation and complete transcriptional silencing of cancer genes persist after depletion of EZH2

Kelly M. McGarvey; Eriko Greene; Jill A. Fahrner; Thomas Jenuwein; Stephen B. Baylin

doi:10.1158/0008-5472.CAN-06-2029

DNA methylation and complete transcriptional silencing of cancer genes persist after depletion of EZH2

Kelly M. McGarvey, Eriko Greene, Jill A. Fahrner, Thomas Jenuwein, Stephen B. Baylin

School of Medicine

Research output: Contribution to journal › Article › peer-review

89 Scopus citations

Abstract

Recent work suggests a link between the polycomb group protein EZH2 and mediation of gene silencing in association with maintenance of DNA methylation. However,we show that whereas basally expressed target cancer genes with minimal DNA methylation have increased transcription during EZH2 knockdown,densely DNA hypermethylated and silenced genes retain their methylation and remain transcriptionally silent. These results suggest that EZH2 can modulate transcription of basally expressed genes but not silent genes that are densely DNA methylated.

Original language	English (US)
Pages (from-to)	5097-5102
Number of pages	6
Journal	Cancer Research
Volume	67
Issue number	11
DOIs	https://doi.org/10.1158/0008-5472.CAN-06-2029
State	Published - Jun 1 2007

ASJC Scopus subject areas

Oncology
Cancer Research

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10.1158/0008-5472.CAN-06-2029

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AU - Jenuwein, Thomas

AU - Baylin, Stephen B.

PY - 2007/6/1

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AB - Recent work suggests a link between the polycomb group protein EZH2 and mediation of gene silencing in association with maintenance of DNA methylation. However,we show that whereas basally expressed target cancer genes with minimal DNA methylation have increased transcription during EZH2 knockdown,densely DNA hypermethylated and silenced genes retain their methylation and remain transcriptionally silent. These results suggest that EZH2 can modulate transcription of basally expressed genes but not silent genes that are densely DNA methylated.

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DNA methylation and complete transcriptional silencing of cancer genes persist after depletion of EZH2

Abstract

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