TNFa-producing Macrophages Determine Subtype Identity and Prognosis via AP1 Enhancer Reprogramming in Pancreatic Cancer [i4C-seq]

According to our previous data, BRD4 controls the inflammatory cJUN transcription factor via enhancer interaction to promote a basal-like phenotype in pancreatic cancer. Therefore, in this study, we wanted to asses BRD4-mediated 3D chromatin interactions at a potential cJUN enhancer locus in pancreatic cancer. Hence, we performed i4C-seq in PANC1 cells in absencece and presence of the BET/BRD4 inhibitor JQ1 for this site. Overall design: i4C-seq was performed in PANC1 cells treated with JQ1 or DMSO control. A viewpoint around a cJUN enhancer site was used.