Fig. 3

A PITPNC1 gene signature features KRAS-regulated genes and predicts poor LUAD and PDAC patients’ outcome. A Heat map of downregulated and upregulated genes in A549 cells after PITPNC1 inhibition with two specific shRNAs (sh6 and sh7) or control (GFPsh). B Gene set enrichment analysis (GSEA) of the dPITPNC1 gene signature in the comparison of both genetically and pharmacologically KRAS inhibition (tet-shKRAS, activated by 1 µg/ml doxycycline, or KRASiARS1620 respectively) vs control (GFP or DMSO respectively). C GSEA of the dPITPNC1 gene signature in the comparison of gene expression data from cancer cell lines (iKrasC) and xenograft tumours (iKrasT) derived from an inducible genetically engineered mouse (GEM) model of Kras-driven PDAC in which doxycycline administration activates expression of a mutant Kras allele. D GSEA of the dPITPNC1 gene signature in the comparison of mut vs wt KRAS LUAD in four data sets. E GSEA of the dPITPNC1 gene signature in the comparison of PDAC vs normal tissue in two data sets. F Survival analysis of LUAD patients (TCGA data set) stratified by the dPITPNC1 gene signature (Log-rank test p = 0.0059). G Survival analysis of LUAD patients (Shedden et al. data set) stratified by the dPITPNC1 gene signature (Log-rank test p = 0.01772). H Survival analysis of PDAC patients (ICGC data set) stratified by the dPITPNC1 gene signature (Log-rank test p = 0.0081). I Survival analysis of PDAC patients (TCGA data set) stratified by the dPITPNC1 gene signature (Log-rank test p = 0.0137)