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. 2019 Jul 22;38:324. doi: 10.1186/s13046-019-1284-y

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© The Author(s). 2019

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 3 — HERG1 enhances migration and invasion of TE-1 and KYSE-30 cells. a Cell migration was assessed in wound healing assays. After 24 h, the wound was nearly closed upon HERG1 overexpression in TE-1 cells and was wider following HERG1 knockdown in KYSE-30 cells (n = 3). b In Boyden chamber invasion transwell assays, invasiveness was quantified by counting the cells invading through Matrigel into the bottom chamber (n = 3). c and d mRNA and protein levels of HERG1, E-cadherin, vimentin, and fibronectin in the different treatment groups were analyzed by qPCR (c) and western blotting (d); n = 3. (e) qPCR results showed that the expression of HERG1 was significantly correlated with that of the EMT markers, E-cadherin, vimentin, and fibronectin in samples of patients with ESCC; n = 20. *: p < 0.05