ChIP-Seq N8 S159

To understand the manner by which RAR and RXR program cell state transitions, we performed ChIP-seq to identify their compendium of target genes in an unbiased manner. We exposed the mesenchymal NAMEC8 and SUM159 cancer cells to retinoid treatment, followed by the genome-wide analyses of target gene binding sites for RXR, RAR, H3K27ac and p300. Exposure to bexarotene, a RXR ligand, led to a subset of genes that became bound by RXR, as well as RAR, since both could form heterodimers. These genes furthermore showed increases in p300 binding, and H3K27ac (histone 3, lysine 27 acetylation) modification, which marks gene enhancers. Overall design: NAMEC8 and SUM159 were treated with DMSO or Bexarotene for 7days (ST) and 14 days (LT). They were then harvested and examined with 4 different antibodies.