Mutant GNAS drives pancreatic tumorigenesis by inducing PKA-mediated SIK suppression and reprogramming lipid metabolism

Gain-of-function mutation of GNAS is frequently observed in pancreatic and other gastrointestinal cancers. Aim of this study was to delineate the oncogenic mechanisms downstream of mutant GNAS. To gain insight into the expression of different transcripts, we perforemd RNA-sequencing (RNA-seq) studies. For this total RNA was isolated in duplicate from two independent KRAS,GNAS mutant lines (A and B) grown in 3D culture with doxycycline supplementation. RNA samples were prepared using Illumina TruSeq RNA Sample Preparation Kit v2 and sequenced using an Illumina HiSeq 2500 sequencer, generating 50-bp single-end reads. Data was processed using a standard RNA-seq pipeline that used Tophat2 to align the reads to mm9, and the Cufflinks suite to calculate FPKM values. Our results shows level of RNA expression in KRAS, GNAS mutant cells. RNA profiles of KGC 3D cultures were generated by deep sequencing, in duplicate in two different lines by Illumina HiSeq 2500 sequencer.