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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. 5 — Whole-transcriptome sequencing reveals that AKR1B10 is a target of METTL3. A Volcano plots showing DEGs between METTL3-overexpressed and Vector groups by transcriptome sequencing in RBE cells (n = 3). Red dots means gene upregulated in METTL3-overexpressed group compared with the Vector group, such as AKR1B10; green dots means downregulated in METTL3-overexpressed group compared with the Vector group. B Bubble plot of KEGG enrichment of the upregulated DEGs between the METTL3-overexpressed and Vector groups in RBE cells. C RT‒qPCR verification of transcriptome sequencing results. Four upregulated DEGs between the METTL3-overexpressed and Vector groups were selected. D The results of MeRIP-qPCR in the OE-METTL3 and Vector groups for four candidate DEGs. E The protein expression of AKR1B10 in RBE cells upon METTL3 overexpression was detected by western blotting. F Five potential m6A modification sites on AKR1B10 mRNA predicted by the SRAMP database. G The binding relationship between METTL3 and AKR1B10 was detected by RIP assays. H The effect of METTL3 overexpression on the stability of AKR1B10 mRNA was measured by actinomycin D. I The m6A modification site of METTL3 on AKR1B10 mRNA was explored by using a luciferase reporter assay. ns means P > 0.05, *Means P < 0.05, **means P < 0.01, ***means P < 0.001