SRA

Our initial data showed different responses of abl and DU145 cells to EZH2 inhibitors, therefore we detected the chromatin binding signals of H3K27me3 in both cell lines in the presence of the compounds. We found that genome-wide changes in H3K27me3 levels were not associated with the inhibitor-mediated transcriptional programs or biological effects. Since the gene expression profiles upon the compound treatment indicated an important role of AR signaling in mediating the inhibitory action of the drugs in abl cells, we them mapped AR chromatin binding patterns in the presence or absence of EZH2 inhibitors. It was interesting to detect a dramatic decline in AR binding intesities at regulatory regions of the regulated target genes. Overall design: Detection of the changes in chromatin binding intesities/signals of H3K27me3 and AR upon EZH2 inhibitors in prostate cancer cells