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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. 6 — Aberrant expression of DLEU2 drives EMT and glycolysis in EC. a Morphological changes upon functional overexpression or inhibition of DLEU2. b Western blotting analysis of the indicated proteins in EC cells following overexpression or knockdown of DLEU2. c, d, e Cell migration (c), invasion (d), sphere formation (e) of EC cells upon overexpression or inhibition of DLEU2. f Cell glucose consumption and lactate production of Ishikawa cells following overexpression of HK2. g Cell viability assay to assess the effects of DLEU2 knockdown on the cellular response to TX. Ishi: Ishikawa; vec: vector; sh: shRNA. *P < 0.05