GSE160856
ERbeta influencing p65 cistromes in colon cancer cells
Inflammation is involved in both initiation and promotion of colorectal cancer (CRC), and patients with inflammatory bowel disease (IBC) have increased risk of developing CRC. Tumor necrosis factor alpha (TNFa) is a cytokine secreted by e.g. macrophages, and this signaling is deregulated in IBD and CRC. TNFa activates the pro-survival transcription factor complex NF?B, which is composed of several subunits including p65 (RELA). We recently characterized the genome-wide transcriptional impact by TNFa in two CRC cell lines, but how p65 binds the chromatin, its cistrome, in colorectal cancer cells has not been explored. We here used p65 chromatin immunoprecipitation followed by sequencing (ChIP-Seq) in HT29 and SW480 cells, and correlated with the transcriptomic impact of TNFa. Further, estrogen receptor beta (ERß) has anti-inflammatory and anti-tumorigenic effects in colon cells and interacts with NF?B main targets. We have shown that ERß impacts TNFa signaling in CRC cells and ERß impacts the P65 cistrome. Overall design: ChIP-Seq was performed in CRC engineered cell lines re-expressing ERß and mock (emply vector without ERß).Each ChIP was performed three times. For further analysis, we focused on sites present in at least two out of three replicates.