Transcription factors enriched in tumor-associated enhancers in VHL-deficient ccRCC

VHL loss is the most common genetic alteration event in ccRCC. We profiled histone modifications from VHL-deficient ccRCC primary tumors and cell lines. We show that ccRCCs exhibit a pervasive gain of enhancers around hypoxic and metabolic transcriptional targets. Motif analysis using HOMER revealed significant enrichment of AP-1, ETS, NF?B and HIFa in tumor enhancers. We generated ChIP-seq binding data for c-Jun, ETS1, NF?B, and P300, a histone acetyltransferase, in 786-O cells. ChIP-seq profiles of HIF2a and HIF1ß in 786-O were already generated previously (GSE34871) Overall design: Transcription factor ChIP-Seq in ccRCC cell lines