Skip to main content
Fig. 9 | Genome Biology

Fig. 9

From: VULCAN integrates ChIP-seq with patient-derived co-expression networks to identify GRHL2 as a key co-regulator of ERa at enhancers in breast cancer

Fig. 9

Changes in H3K27ac on knockdown of GRHL2. (a) The effect of silencing GRHL2 on H3K27ac at 48 h in MCF7 and T47D cell lines was monitored by ChIP-seq. Analysis of sites proximal to TFF1, XBP1, and GREB1 showed significant changes in acetylation at all three sites in MCF7. Significant changes were only found at GREB1 in T47D (top right). While XBP1 and GREB1 show an increase in histone acetylation on silencing GRHL2, TFF1 showed the reverse effect. (b) Genome-wide, the effects of silencing GRHL2 led to a significant redistribution of H3K27ac in both the MCF7 and T47D cell lines, with both showing an increase and decrease in the histone mark dependent on site. c From left to right. Coverage as calculated by Homer. H3K27ac was found at GRHL2 sites in both MCF7 and T47D cells, in particular at the E2-responsive sites. The same mark was also found at P300 sites as expected. Analysis of ER binding at H3K27ac sites showed an enrichment for ER binding at the H3K27ac sites that were most responsive to knockdown of GRHL2 in MCF7 cells

Back to article page