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. 2023 Mar 28;14(3):221. doi: 10.1038/s41419-023-05715-1

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© The Author(s) 2023, corrected publication 2022

Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 3 — A The intersection between the list of predicted m6A targets of METTL3 by m6A2target, the list of differentially expressed genes in GEM-resistant pancreatic cancer, and the list that contained genes correlated with METTL3 expression showed the potential direct downstream targets of METTL3 in pancreatic cancer. B The relative mRNA expression of the identified five genes: SETD1A, ZNF777, CIC, DDX23, and RBM14 in cells with METTL3 silence. **P < 0.01, ***P < 0.001, compared with the sh-NC group. C, D The expression of DDX23 mRNA in the two cell lines with METTL3 knockdown (C) and METTL3 overexpression (D) was analyzed by qRT-PCR. C ***P < 0.001, compared with the sh-NC group. D **P < 0.01, compared with the vector group. E, F The expression of DDX23 protein in the two cell lines with METTL3 knockdown (E) and METTL3 overexpression (F) was determined using western blotting. G The m6A level of DDX23 in pancreatic cell lines with METTL3 knockdown (left panel) and overexpression (right panel) was measured. ***P < 0.001, compared with the sh-NC group; **P < 0.01, compared with the vector group. H The half-life of DDX23 mRNA in cells with respective METTL3 knockdown and overexpression with Actinomycin treatment was analyzed using qRT-PCR. I The regulatory relationship between METTL3 and DDX23 mRNA was validated using the dual-luciferase reporter gene assay. J In TCGA pancreatic cancer data, METTL3 and DDX23 were found significantly positively correlated. PAAD: pancreatic adenocarcinoma. K In all the cancers of TCGA, METTL3 expression was found significantly correlated with DDX23 expression. L The FISH assay showed that METTL3 knockdown led to DDX23 downregulation in the pancreatic cancer cell line.