Transcriptomic profiling identifies unique and shared functions of oncogenic KRAS and RIT1

Aberrant activation of RAS oncogenes is a prevalent event in lung adenocarcinoma, with somatic mutation of KRAS occurring in ~30% of tumors. Recently, we identified somatic mutation of the RAS-family GTPase RIT1 in lung adenocarcinoma, but relatively little is known about the biological pathways regulated by RIT1 and how these relate to the oncogenic KRAS network. Here we present (quantitative proteomic and) transcriptomic profiles from KRAS-mutant and RIT1-mutant isogenic lung epithelial cells and globally characterize the signaling networks regulated by each oncogene. Overall design: Whole transcriptome (mRNA) profiles of 18 samples, encompassing five genetic perturbations through lentiviral transduction of wild-type or variant vectors (KRAS WT, KRAS G12V, KRAS Q61H, RIT1 WT, RIT1 M90I), as well as one control plasmid vector (Renilla). Sequenced in triplicate on Illumina NovaSeq.