MYC controls a double-stranded RNA-dependent autocrine pathway that links nuclear mRNA splicing to pro-inflammatory signaling in pancreatic carcinoma

The oncogene MYC supresses TBK1 activity in a KRAS/mutant p53-driven pancreas carcinoma model and thereby interferes with the signaling that follows recognition of dsRNA species by the pattern recoginition receptor TLR3, allowing the tumor cells to evade recognition by the immune system. 4SU-seq and RNA-seq experiments to determine nascent RNA synthesis and global gene expression after MYC knockdown, after TBK1 knockout, after MycWT or MycVD overexpression and after overexpression of an IKBa mutant in a pancreatic carcinoma model system (KPC) in vitro and in vivo.