Smad4 restricts injury-provoked biliary proliferation and carcinogenesis (AKPS_EV_vs_Smad4_RNAseq)
RNA-sequencing of TGFß treated empty vector (EV) or Smad4-expressing AKPS lines followed by GSEA revealed a number of gene sets overlapping with those obtained from analyses in reactive cholangiocytes. Hallmark gene sets MYC, E2F, G2M checkpoint, and oxidative phosphorylation were enriched with loss of Smad4, while TGFß signaling, EMT, and TNFa were enriched with intact Smad4 signaling, suggesting conserved growth suppressive functions of Smad4 in primary cholangiocytes and advanced cancer. Overall design: Comparative gene expression profiling analysis of RNA-seq data for TGFß treated empty vector (EV) or Smad4-expressing AKPS lines