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. 2019 Feb 15;10(3):150. doi: 10.1038/s41419-019-1332-8

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© The Author(s) 2019

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. 3 — a The migration and invasion abilities were detected by transwell assay in SW620 and LOVO cells after transfection of lncRNA ZNFX1-AS1 siRNAs (*P < 0.05). b The migration was measured by wound healing assay in SW620 cells after transfection of lncRNA ZNFX1-AS1 siRNAs (*P < 0.05). c The cell invasion abilities were measured in SW480 and HT-29 cells after ectopic expression of lncRNA ZNFX1-AS1 (*P < 0.05). d immunofluorescence analysis showed that knockdown of lncRNA ZNFX1-AS1 increased the level of epithelial marker E-cadherin while reduced the level of mesenchymal marker N-cadherin. e real-time PCR showed that knockdown of lncRNA ZNFX1-AS1 increased the level of epithelial markers such as E-cadherin, α-catenin, β-catenin while reduced the level of mesenchymal markers such as N-cadherin, vimetin, snail and slug. f The stable lncRNA ZNFX1-AS1 knockdown SW620 cells were used for the in vivo metastasis assay, the micro-metastasis in the lung and in the liver from the two groups were shown (*P < 0.05)