LIFR antagonism reverses epithelial pro-CAF programs in pancreatic ductal adenocarcinoma

In PDAC cancer cells, MIAPaCa-2 cells, LIF induced a coordinated transcriptional network encompassing inflammatory mediators, paracrine fibroblast-activating signals and ECM/mechanotransductive modules, while repressing stromal-inhibitory genes. These signatures were recapitulated in PDAC tissues, where LIF expression directly correlated with CAF, iCAF and myCAF markers and with stromal remodelling genes.