Fig. 3: The ETS2-SE is highly disease-specific in both CRC and IBD and its activity is strongly correlated with the expression level of ETS2 in CRC.

A Overlayed IGV tracks showing the H3K27ac (n = 72) and H3K4me3 (n = 42) ChIP-seq profiles in paired normal colon (gray) and primary CRC samples (red) across the ETS2 promoter and its distal SE. B Quantification of the ChIP-seq signal (RPGC in a bin size of 10 bp) from samples described in (A) at ETS2 promoter or its distal SE. C Scatter plots showing the correlation between ETS2 expression level and H3K27ac level at ETS2-SE or ETS2 promoter in primary CRC or normal colon tissues. PCC Pearson Correlation Coefficient. D IGV tracks showing the H3K27ac ChIP-seq and RNA-seq profiles in normal colon tissue (N) or primary tumor (T) from two CRC patients at indicated regions. Loci of active enhancer transcription in CRC were indicated by black arrows. E Upper panel: IGV tracks showing the overlayed H3K27ac ChIP-seq profiles in normal colon tissue (n = 5, gray) or UC colon tissue (n = 5, dark green) at indicated regions. Bottom panel: 5’ CAGE peaks labeling active transcription events from two representative UC and CD samples. The position of a known IBD-risk SNP was indicated by green rectangle in shadow. F Results of eQTL analysis in primary CRCs showing differential ETS2 expression level in samples with different risk SNP genotype.