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. 2021 Jun 26;40:216. doi: 10.1186/s13046-021-02018-1

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© The Author(s) 2021

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. 2 — HK2 promotes the EMT phenotypes in EC cells. a qRT-PCR analysis of HK2 expression in EC cells after overexpression or knockdown of HK2. b Western blotting analysis of HK2, E-cadherin (CDH1), and Vimentin expression in EC cells transfected as indicated. c HK2 affects EC cell morphology. d, e, f Migration (d), invasion (e), and sphere formation (f) of EC cells after overexpression or knockdown of HK2. g Cell survival was examined by a cell viability assay in EC cells transfected as indicated and treated with TX. h A heat map of qRT-PCR results shows the expression of the indicated genes in EC cells upon overexpression or knockdown of HK2. Red: upregulation; blue: downregulation. Ishi: Ishikawa; vec: vector; sh: shRNA. *P < 0.05