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. 2020 Apr 8;11(4):225. doi: 10.1038/s41419-020-2422-3

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 5 — A Western blotting analysis of ZNF703, CLDN4, E-cadherin, N-cadherin, Vimentin, and ZEB1 expression in upregulating or downregulating CLDN4 in the SMMC7721-ZNF703 or HCCLM3-shZNF703 cells, respectively. B Transwell (B1) and wound-healing (B2) assays demonstrate that upregulation of CLDN4 increases migration and invasion abilities of HCCLM3-shZNF703 cells, whereas downregulation of CLDN4 decreases migration and invasion abilities of SMMC7721-ZNF703 cells. Scale bars: 250 μm (wound-healing) and 75 μm (transwell). C In vivo metastasis assays, (C1) Lung representative morphology and H&E staining, (C2) incidence of lung metastasis, (C3) number of metastatic lung foci, and (C4) overall survival of nude mice in SMMC7721-ZNF703 cells downregulating CLDN4 and HCCLM3-shZNF703 cells upregulating CLDN4 groups (n = 10) are shown. Scale bars: 250 μm (low magnification) and 100 μm (high magnification). Data are presented as mean ± S.D for three independent experiments. *P < 0.05.