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. 2019 Jul 25;42(4):1380–1390. doi: 10.3892/or.2019.7250

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Copyright: © Yue 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 4. — CLIC1 is involved in the miR-124-induced inhibition of liver cancer cell migration and invasion. (A) Scratch wound-healing motility assay of liver cancer cells transfected with miR-124, miR-124-NC, miR-124 + CLIC1 and miR-124 + vector control. Scale bar, 200 µm. (B) The Transwell assay without Matrigel coating showed the cell migration ability of liver cancer cells co-transfected with miR-124 and CLIC1 expression vector compared with the controls. Scale bar, 200 µm. (C) Cell invasion ability of liver cancer cells co-transfected with miR-124 and CLIC1, evaluated by Matrigel-coated Transwell assay. Scale bar, 200 µm. ^***P<0.001. NC, negative control; CLIC1, chloride intracellular protein 1; miR, microRNA.

Figure 4. — CLIC1 is involved in the miR-124-induced inhibition of liver cancer cell migration and invasion. (A) Scratch wound-healing motility assay of liver cancer cells transfected with miR-124, miR-124-NC, miR-124 + CLIC1 and miR-124 + vector control. Scale bar, 200 µm. (B) The Transwell assay without Matrigel coating showed the cell migration ability of liver cancer cells co-transfected with miR-124 and CLIC1 expression vector compared with the controls. Scale bar, 200 µm. (C) Cell invasion ability of liver cancer cells co-transfected with miR-124 and CLIC1, evaluated by Matrigel-coated Transwell assay. Scale bar, 200 µm. ^***P<0.001. NC, negative control; CLIC1, chloride intracellular protein 1; miR, microRNA.