Transcriptional responses of autophagy proficient and deficient pancreatic tumors and cells treated with TNFa

Pancreatic ductal adenocarcinoma (PDAC) cells require substantial metabolic rewiring to overcome nutrient limitations and immune surveillance. However, the metabolic pathways necessary for pancreatic tumor growth in vivo are poorly understood. To address this, we performed metabolism-focused CRISPR screens in PDAC cells grown in culture or engrafted in immunocompetent mice. While most metabolic gene essentialities are unexpectedly similar under these conditions, a small fraction of metabolic genes are differentially required for tumor progression. Our screens identify autophagy as a metabolic requirement for pancreatic tumor immune evasion. Mechanistically, autophagy protects cancer cells from CD8+ T cell killing through TNFa-induced cell death in vitro. This data set contains RNA-seq data of KP pancreas Atg7_KO cells expressing empty vector or Atg7 cDNA. These cells were grown as subcutaenous tumors and also cultured in vitro with and without TNFa. Overall design: RNA sequencing: KP panc Atg7_KO cells expressing empty vector or Atg7 cDNA. Cells were grown as subcutaneous tumors in C57BL/6J mice or in vitro with or without TNFa. Three replicates were done for each condition.