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. 2020 Jan 23;43(3):919–929. doi: 10.3892/or.2020.7478

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Copyright: © Hu et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 5. — SLCO4C1 downregulation suppresses the migration and invasion abilities of HEC-1A and RL95-2 cells and affects the EMT phenotype in EC cells. (A) Migration of HEC-1A and RL95-2 cells transfected with siNC, siSLCO4C1-1 or siSLCO4C1-2 by wound healing assay at 0 and 48 h. (B) Invasion of HEC-1A and RL95-2 cells transfected with siNC or siSLCO4C1-1 by Transwell assay. (C) Epithelial morphology induced by the suppression of SLCO4C1 in HEC-1A and RL95-2 cells (magnification, ×400). (D) Expression of EMT markers in HEC-1A and RL95-2 cells transfected with siNC, siSLCO4C1-1 or siSLCO4C1-2 by western blotting. GAPDH was used as a loading control. The results were determined from triplicate experiments and the error bars represent the mean ± SD. *P<0.05, **P<0.01, ***P<0.001 vs. the Ctrl group and siNC group. SLCO4C1, solute carrier organic anion transporter family member 4C1; EMT, epithelial-mesenchymal transition; EC, endometrial cancer.