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-2a mRNA in renal cancer. Epigenetic analysis of the EPAS1 locus (coding for HIF-2a) using ATAC-seq, ChIP-seq and RNA-seq revealed an oncogenic enhancer that maintains a HIF-dependent feed-forward circuit of HIF-2a regulation in renal tumor cells. Overall design: This study consists of ATAC-seq, ChIP-seq, CUT&Tag-seq and RNA-seq samples from primary tubular and primary ccRCC cells as well as genetically modified 786-0 and RCC4 cells. *************************************************************** Access to unprocessed raw data of primary cells is restricted to protect the privacy and intent of research participants consistent with the informed consent agreements provided by individual research participants. ***************************************************************