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. 2022 Dec 7;22:385. doi: 10.1186/s12935-022-02809-2

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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. 8 — METTL3 exerts an oncogenic role in CCA through AKR1B10. A The proliferation of RBE cells after knockdown of AKR1B10 upon METTL3 overexpression was detected by CCK8 assay. B Statistical results of Transwell assays. The numbers of migrating and invading cells were counted for comparison. C The migration and invasion of RBE cells after knockdown of AKR1B10 upon METTL3 overexpression were detected by Transwell assays. Scale bar: 100 μm. D Glucose uptake of RBE cells after knockdown of AKR1B10 upon METTL3 overexpression was detected using a commercial kit. E Lactate production in RBE cells after knockdown of AKR1B10 upon METTL3 overexpression. *Means P < 0.05, **means P < 0.01, ***means P < 0.001