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. 2020 Nov 3;21(1):6. doi: 10.3892/ol.2020.12267

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Copyright: © Liu 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 2. — TRIM59 knockdown inhibits hESC cell migration and invasion. TRIM59 protein expression levels were (A) determined via western blotting and (B) semi-quantified. (C) At 48 h post-transfection, TRIM59 mRNA expression levels were measured via reverse transcription-quantitative PCR. At 48 h post-transfection, TRIM59 protein expression levels were (D) determined via western blotting and (E) semi-quantified. The effect of TRIM59 knockdown on hESC cell proliferation was (F) determined by performing a colony formation assay (scale bar, 200 µm) and (G) quantified. The effect of TRIM59 knockdown on hESC cell migration was (H) assessed by performing a wound healing assay (scale bar, 200 µm) and (I) quantified. (J) Eca109 cell viability was measured at different time points using a Cell Counting Kit-8 assay. (K) The effect of TRIM59 knockdown on MMP2 and MMP9 mRNA expression levels. The effect of TRIM59 knockdown on MMP2 and MMP9 protein expression levels was (L) assessed via western blotting and (M) semi-quantified. *P<0.05 vs. Eca109 or siNC. TRIM59, tripartite motif-containing 59; hESC, human esophageal cancer; MMP, matrix metallopeptidase; si, small interfering RNA; NC, negative control; WT (function as an ineffective proof of siNC), wild-type; OD, optical density.