Fig. 7. OSM drives tumour growth and metastasis in vivo.

a Left: Representative iRFP imaging of resected pancreatic tumours from orthotopically transplanted immune-competent wildtype (Wt) (n = 19) and Osm^−/− (n = 13) mice. Right: Quantification of iRFP signal intensity, tumour volume and tumour weight. Results displayed as mean ± SEM (Wt, n = 19 and Osm^−/− n = 13), two-tailed student t test. b Left: Representative Pan-Cytokeratin (PanCK) staining of wildtype and Osm^−/− tumour sections. Right: Quantification of total PanCK^pos staining, mesenchymal PanCK^pos staining, and epithelial PanCK^pos staining following morphology analysis, and the epithelial–mesenchymal PanCK^pos ratio in tumour sections from wildtype (n = 6) and Osm^−/− (n = 6) mice. A shift of PanCK^pos cells from a mixed mesenchymal and epithelial morphology in wildtype tumours to a more epithelial-dominant morphology in Osm^−/− animals. Results displayed as mean ± SEM, two-tailed student t test. c Quantification of total Ki67,^pos CD31^pos, and SLUG^pos immunohistochemical staining of tumour sections from wildtype (n = 6) and Osm^−/− (n = 6) mice. Results displayed as mean ± SEM, two-tailed student t test. d Upper: Representative iRFP in vivo imaging (top) and haematoxylin and eosin staining (bottom) of resected livers from wildtype and Osm^−/− mice. Lower: Quantification of iRFP^pos liver metastasis incidents in wildtype (n = 11/19) and Osm^−/− (n = 0/13) animals. e Model outlining heterocellular OSM–OSMR signalling between pancreatic cancer cells, fibroblasts and macrophages. Pancreatic cancer cell secretion of GM-CSF induces macrophage secretion of OSM, which reprograms fibroblasts to an inflammatory phenotype, in turn accentuating tumour growth and metastasis. Also see Supplementary Fig. 8. Source data are provided as a Source Data file.