Coordinated transcriptional and catabolic programs support iron dependent adaptation to RAS-MAPK pathway inhibition in pancreatic cancer [ChIP-Seq]

In this study, human pancreatic ductal adenocarcinoma cells lines (KP4, MiaPaca2) were treated with the MEK inhibitor, Trametinib or DMSO for 48hrs prior to RNA-seq profiling to evaluate significant gene expression changes associated with MEK inhibition. To assess the role of transcription factors MYC and TFE3 in regulation of gene expression changes associated with MEK inhibition, we performed chromatin immunoprecipitation using antibodies against c-MYC and TFE3 in KP4 cells following 48hrs of Trametinib or DMSO treatment. Overall design: Human pancreatic cancer cell, KP4 was treated with DMSO or 100nM Trametinib for 48h and chromatin immunoprecipitation was performed for c-MYC and TFE3.