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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. 3 — AKR1B10 promotes glycolysis and the malignant phenotype of CCA cells in vitro. A The overexpression efficacy of METTL3 mRNA expression in RBE cells was confirmed by RT‒qPCR. B The overexpression efficacy of METTL3 protein expression in RBE cells was confirmed by western blot. C The proliferation of RBE cells after overexpression of METTL3 was detected by CCK8. D TUNEL staining was used to detect RBE cell apoptosis after overexpression of METTL3. Scale bar: 50 μm. E The migration and invasion of RBE cells after overexpression of METTL3 were detected by Transwell assays. The numbers of migrating and invading cells were counted for comparison. Scale bar: 100 μm. F Glucose uptake of RBE cells after overexpression of METTL3 was detected using a commercial kit. (G) Lactate production in RBE cells after overexpression of METTL3. **Means P < 0.01, ***means P < 0.001