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. 2022 Jun 15;20:87. doi: 10.1186/s12964-022-00898-0

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© The Author(s) 2022

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. 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 in a credit line to the data.

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Fig. 3 — NEK2 regulated expression of YAP1 and affected EMT of ESCC in vitro. A Silence NEK2 with two shRNA both decreased the expression of YAP1 and EMT biomarkers like N-cadherin and Vimentin. B Overexpression of NEK2 enhanced the migration in ESCC by Transwell assay. C Overexpression of NEK2 increased the expression of YAP1, N-Cadherin, and Vimentin. D The impairment of migration caused by Lv-shNEK2 could be partly recovered by the introduction of HA-YAP1 in Eca-109. E The reduction of N-Cadherin and Vimentin due to knockdown of NEK2 could be incompletely rescued with the elevation of YAP1 in Eca-109. All images represented one of three independently repeated experiments. **P < 0.01, ***P < 0.001