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. 2020 Jun 16;12(6):1590. doi: 10.3390/cancers12061590

Figure 3.

Figure 3

MSI-N1014 treatment prevented cancer-associated fibroblast (CAF) transformation. (A) Representative immunofluorescence images of CAFs transformed by MSI-1014-treated DLD1 and HCT116 cells. Reduced expression of alpha-smooth muscle actin (α-SMA) was observed. (B) ELISAs showed reductions in interleukin (IL)-6, and vascular endothelial growth factor (VEGF) released by CAFs generated by co-culturing with MSI-N1014-treated DLD1 and HCT116 cells. MSN-N1014-treated CRC cells showed reduced migratory (C) and tumor sphere-generating abilities (D). (E) Western blot analysis showing that there were increased expressions of epidermal growth factor receptor (EGFR), mammalian target of rapamycin (mTOR) (oncogenic markers), leucine-rich repeat-containing G-protein coupled receptor 5 (LGR5), and β-catenin (stemness markers), and increased ATP-binding cassette super-family G member 2 (ABCG2) expressions and IL-6 (an inflammatory marker) in CRC and tumor-sphere cells. However, after MSI-N1014 treatment, these markers were significantly suppressed. Numbers in red indicate the relative expression ratio. * p < 0.05, ** p < 0.01, *** p < 0.001.