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. 2020 Jul 9;10(19):8790–8806. doi: 10.7150/thno.44456

Figure 7.

Figure 7

Chrysin inhibits the EMT of colorectal cancer. (A) Cell phenotypic changes in HCT116 cells treated with 20 µM Chrysin. (B) WB analysis of COMP and EMT-related markers in HCT116 cells treated with different concentrations of Chrysin. (C) Matrigel invasion assay of HCT116, HCT-8, and SW620 cells treated with different concentrations of Chrysin. (D) Cell wound scratch assay of HCT116, HCT-8, and SW620 cells treated with different concentrations of Chrysin. (E) E-cadherin and Vimentin immunofluorescence assays after Chrysin treatment of colorectal cancer cells for 24 h. (F) HCT116 and HCT-8 cells were injected to nude mice subcutaneously and treated with Chrysin. Tumor volumes were measured every 4 days. (G) Tumor weight in the control, Chrysin, and Chrysin+shCOMP groups. (H) The in situ spleen model of the colorectal cancer cell line SW620 showed that Chrysin inhibited liver metastasis of colorectal cancer. (I) Immunohistochemical staining to identify EMT biomarkers and COMP-related proteins in the control, Chrysin, and Chrysin+shCOMP groups. (J) Staining indices of COMP, E-cadherin, Vimentin, Snail1, Twist1, and MMP2 in the control, Chrysin, and Chrysin+shCOMP groups. The error bars in all graphs represented SD, and each experiment was repeated three times. * and ** stand for P<0.05 and P<0.01, respectively.