Frequent switching of Polycomb repressive marks and DNA hypermethylation in the PC3 prostate cancer cell line

• DOI: 10.1073/pnas.0806437105
• Publication Date: 2008-08-28T01:39:48Z
• Authors: Einav Nili Gal-Yam; Gerda Egger; Leo Iniguez; Heather Holster; Steingrímur Einar...; Xinmin Zhang; Joy C. Lin; Gangning Liang; Peter A. Jones; Amos Tanay
• Keywords: Reprogramming; Epigenomics; Epigenome; CpG site; Cancer Epigenetics; PRC2

Epigenetic reprogramming is commonly observed in cancer, and hypothesized to involve multiple mechanisms, including DNA methylation Polycomb repressive complexes (PRCs). Here we devise a new experimental analytical strategy using customized high-density tiling arrays investigate coordinated patterns of gene expression, methylation, marks which differentiate prostate cancer cells from their normal counterparts. Three major changes the epigenomic landscape distinguish two cell types. Developmentally significant genes containing CpG islands are silenced by PRCs acquire silencing lose PRC (epigenetic switching). Because these normally silent this switch does not cause de novo repression but might significantly reduce epigenetic plasticity. Two other groups either without occupancy (5mC reprogramming) or (PRC reprogramming). Our data suggest that mechanisms act parallel reprogram epigenome hypermethylation may replace Polycomb-based near key regulatory genes, possibly reducing