2006
DOI: 10.1038/ng1950
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Polycomb-mediated methylation on Lys27 of histone H3 pre-marks genes for de novo methylation in cancer

Abstract: Many genes associated with CpG islands undergo de novo methylation in cancer. Studies have suggested that the pattern of this modification may be partially determined by an instructive mechanism that recognizes specifically marked regions of the genome. Using chromatin immunoprecipitation analysis, here we show that genes methylated in cancer cells are specifically packaged with nucleosomes containing histone H3 trimethylated on Lys27. This chromatin mark is established on these unmethylated CpG island genes e… Show more

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Cited by 1,083 publications
(935 citation statements)
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References 29 publications
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“…Chromatin state analysis revealed that the hypermethylation‐associated H3K27me3 and H3K4me1/3 marks configured bivalent chromatin domains, as has been extensively described in embryonic stem cells (Fernández et al., 2015; Ohm et al., 2007; Rakyan et al., 2010; Schlesinger et al., 2007; Teschendorff et al., 2010; Widschwendter et al., 2007). Moreover, our data reveal that this chromatin signature is not restricted to only embryonic stem cells, but rather this trend should be considered an extended, global tissue‐independent chromatin signature of DNA hypermethylation in aging and cancer.…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…Chromatin state analysis revealed that the hypermethylation‐associated H3K27me3 and H3K4me1/3 marks configured bivalent chromatin domains, as has been extensively described in embryonic stem cells (Fernández et al., 2015; Ohm et al., 2007; Rakyan et al., 2010; Schlesinger et al., 2007; Teschendorff et al., 2010; Widschwendter et al., 2007). Moreover, our data reveal that this chromatin signature is not restricted to only embryonic stem cells, but rather this trend should be considered an extended, global tissue‐independent chromatin signature of DNA hypermethylation in aging and cancer.…”
Section: Discussionmentioning
confidence: 99%
“…However, the underlying molecular mechanisms governing this relationship are still poorly understood. Recent research has established polycomb‐target gene promoter hypermethylation as a common epigenetic characteristic of cancer (Schlesinger et al., 2007; Widschwendter et al., 2007). In this scenario, prior to alteration these promoters display an embryonic stem cell “bivalent chromatin pattern” consisting of the repressive histone mark H3K27me3 and the active mark H3K4me3 (Ohm et al., 2007).…”
Section: Introductionmentioning
confidence: 99%
“…It has also been shown that genes affected by de novo DNA methylation during tumorigenesis are pre-marked by histone H3 lysine 27 trimethylation, suggesting that this chromatin modification functions as an instructive mechanism in the establishment of cancerspecific DNA methylation patterns Schlesinger et al, 2007;Widschwendter et al, 2007). Of note, H3K27 trimethylation is also an important component of 'bivalent' chromatin structures that are defined by the presence of both activating H3K4 trimethylation and repressive H3K27 trimethylation (Bernstein et al, 2006).…”
Section: Epigenetic Side Effects Of Global Dna Demethylationmentioning
confidence: 99%
“…An exciting recent development in understanding how DNA methylation is targeted to specific tumor suppressor genes in cancer is the discovery that sites that are regionally hypermethylated in cancer are also targets of the histone methyltransferase EZH2 [Vire et al, 2006;Schlesinger et al, 2007]. Interestingly, a very recent article links oncoproteins such as PML-RAR to EZH2 in targeting DNMTs to specific promoters [Marker, 2007].…”
Section: The Relationship Between Chromatin and Dna Methylationmentioning
confidence: 99%