Investigation of bivalently marked promoters in patient-derived colorectal cancer stem cells by ChIP-seq, chromatin accessibility by ATAC-seq, and differential regulation of gene expression following EZH2 inhibition using RNA-seq.. Investigation of bivalently marked promoters in patient-derived colorectal cancer stem cells by ChIP-seq, chromatin accessibility by ATAC-seq, and differential regulation of gene expression following EZH2 inhibition using RNA-seq.

We profiled changes in gene expression following EZH2 inhibition, in a patient-derived, cancer stem cell enriched model. Cells were treated with UNC1999, an EZH2 inhibitor, for 7 days, prior to processing for RNA-seq. In parallel, we identified H3K27me3 and H3K4me3 marked promoters using ChIP-seq at baseline in the same model, as well as chromatin accessibility using ATAC-seq. Overall design: Colorectal cancer stem cells were profiled for bivalently marked (H3K4me3), repressed (H3K27me3) and active (H3K4me3) promoters at baseline. Cells were treated with the EZH2 inhibitor UNC1999, and processed for RNA-seq. ChIP-seq data was used to determine whether the promoters of the differentially regulated genes were marked with repressive, active or bivalent marks. ATAC-seq was performed at baseline to determine chromatin accessibility and used for transcription factor motif analysis. Raw data will be submitted to EGA due to patient privacy concerns.