| Literature DB >> 17200670 |
Yeshayahu Schlesinger1, Ravid Straussman, Ilana Keshet, Shlomit Farkash, Merav Hecht, Joseph Zimmerman, Eran Eden, Zohar Yakhini, Etti Ben-Shushan, Benjamin E Reubinoff, Yehudit Bergman, Itamar Simon, Howard Cedar.
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 early in development and then maintained in differentiated cell types by the presence of an EZH2-containing Polycomb complex. In cancer cells, as opposed to normal cells, the presence of this complex brings about the recruitment of DNA methyl transferases, leading to de novo methylation. These results suggest that tumor-specific targeting of de novo methylation is pre-programmed by an established epigenetic system that normally has a role in marking embryonic genes for repression.Entities:
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Year: 2006 PMID： 17200670 DOI： 10.1038/ng1950
Source DB: PubMed Journal: Nat Genet ISSN： 1061-4036 Impact factor: 38.330