VX-509 attenuates the stemness characteristics of colorectal cancer stem-like cells by regulating the epithelial-mesenchymal transition through Nodal/Smad2/3 signaling

Figure 3 VX-509 inhibits the cancer stem cells characteristics of colorectal cancer-derived cancer stem cells and has an inverse effect on the epithelial-mesenchymal transition progression. A-D: Representative morphology after VX-509 treatment (A, sphere formation assay) or pretreatment (C, sphere recovery assay) and relative statistical analysis (B and D); E: Western blot analysis of Oct4, Nanog, and SOX2 in colorectal cancer (CRC)-derived cancer stem cells (CSCs) treated with different concentrations of VX-509; F: Densitometric analysis of Oct4, Nanog, and SOX2, normalized against β-actin; G: Representative morphology of CRC-derived CSCs in regular 6-well plates after different concentrations of VX-509 treatment; H and I: The effects of different concentrations of VX-509 on the protein expression of E-cadherin, N-cadherin, and vimentin in CRC-derived CSCs were detected by western blot and relative statistical analysis, normalized against GAPDH. Scale bar = 50, 200 μm. n = 3. ^aP < 0.05, ^bP < 0.01, ^cP < 0.001, ^dP < 0.0001 compared to the HCT116 cancer stem cells Mock group and HT29 cancer stem cells Mock group. CSC: Cancer stem cell.