Open chromatin, HIF binding and mRNA expression analysis in primary tubule and ccRCC cells [ChIP-seq]

Inactivation of the von Hippel-Lindau tumor suppressor leads to stabilization of HIF transcription factors and subsequent oncogenic HIF-2 signaling in ccRCC. However, little is known about the transcriptional mechanisms leading to dysregulation of HIF-2α mRNA in renal cancer. Epigenetic analysis of the EPAS1 locus (coding for HIF-2α) using ATAC-seq, ChIP-seq and RNA-seq revealed an oncogenic enhancer that maintains a HIF-dependent feed-forward circuit of HIF-2α regulation in renal tumor cells.