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. 2016 Oct 13;7(47):77306–77318. doi: 10.18632/oncotarget.12639

Figure 4. DcR3 facilitated CRC epithelial-mesenchymal transition.

Figure 4

A. DcR3 overexpression in RKO and HT29 cells caused morphological alteration sresembling EMT, while konckdown of DcR3 in SW480/M5 and HCT116 caused and reverse result. B. The expression of mesenchymal and epithelial markers in RKO and HT29 cells transfected with vector (control) or DcR3 plasmid (DcR3) and SW480/M5 and HCT116 cells transfected of control (shCtrl) or DcR3 shRNA (shDcR3) was detected by western blotting. C. Quantification of protein expression shown in B normalized to α-Tubulin. *P<0.05 compared to control group; n=3. D. Immunostaining of mesenchymal and epithelial markersin RKO and HT29 cells transfected with vector (control) or DcR3 plasmid (DcR3), as indicated. Magnification: 1800x. E. EMT-related protein immunohistochemical staining of primary tumor tissues derived from control or DcR3-containing RKO or HT29 cells, as indicated. Magnification: 200x. F. Quantification of protein expression was assessed by measuring IHC staining intensity. ***P<0.001 compared to control group for each corresponding protein; n=6. DcR3 overexpression in RKO and HT29 increased N-cadherin and vimentin expression and decreased E-cadherin expression.