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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. 4 — NEK2 influenced the oncological effect of ESCC and co-existed with YAP1 in vivo. A Knockdown of NEK2 decelerated the growth rate of Eca-109 in vivo. B Lv-NEK2 group had a compromised manifestation in average radiant efficiency and size than those in the Lv-Con group in vivo imaging. C Knockdown of NEK2 reduced the tumorigenesis of Eca-109 presented in size and weight. D The decreased NEK2 was accompanied by reduced expression and nucleus shuffling of YAP1 by IHC staining. E The downregulated expression of NEK2 simultaneously manifested with less expression and nucleus shuffling of YAP1 by IF imaging. *P < 0.05; IHC immunohistochemistry; IF immunofluorescence