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. 2016 Sep 24;107(10):1443–1452. doi: 10.1111/cas.13024

Figure 5.

Figure 5

Effect of calpeptin on the cancer–stromal interaction between pancreatic cancer cells (PCCs) and pancreatic stellate cells (PSCs). Representative images of migrating PCCs (a) and PSCs (c). (b) PSC supernatant (PSC‐SN) significantly enhanced the migration of PCCs. Calpeptin‐treated PSC‐SN prevented the activation of PCCs stimulated by PSC‐SN. (d) PCC supernatant (PCC‐SN) significantly enhanced the migration of PSCs. Calpeptin‐treated PCC‐SN prevented the activation of PSCs stimulated by PCC‐SN. Effects of calpeptin on gene expression levels of growth factors and ECM proteins associated with cancer–stromal interactions. PCCs (e) and PSCs (f) were untreated (Cont) or treated with calpeptin (Calp). mRNA expression levels were normalized to GAPDH expression and are presented as the fold change in gene expression relative to control PCCs and PSCs. Data are presented as the mean ± SD. ***P < 0.001. Cells were stained with HE; original magnification, ×100. α‐SMA, α‐smooth muscle actin; COL1A1, collagen 1A1; CTGF, connective tissue growth factor; EGF, epidermal growth factor; FGF‐2, fibroblast growth factor‐2; FN1, fibronectin 1; HGF, hepatocyte growth factor; PDGF, platelet‐derived growth factor; POSTN, periostin; TGF‐β1, transforming growth factor‐β1; VEGF, vascular endothelial growth factor.