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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. 1 — A, B. METTL3 was upregulated in GEM-resistant Panc-1 and SW1990 cells. GEM: gemcitabine. A western blotting assay; B fluorescence in situ hybridization (FISH) assay. C The m6A level in GEM-resistant Panc-1 and SW1990 cells was significantly higher than in corresponding parent cells. **P < 0.01, ***P < 0.001, compared with control group. D Both SW1990 and Panc-1 cell lines were sensitive to GEM treatment in a dose-dependent manner whereas GEM-resistant cell lines did not show significant changes across the spectrum of doses of gemcitabine. ***P < 0.001, compared with the corresponding parent cell line. E The two shRNAs against METTL3 inhibited the protein expression of METTL3 in both GEM-resistant cell lines. ***P < 0.001, compared with the GEM-resistant cell line. F The knockdown of METTL3 in GEM-resistant cells significantly increased the sensitivity to gemcitabine treatment and resulted in less cell viability (measured in optical density (OD) at 450 nm). G In both Panc-1 and GEM-resistant Panc-1 cell lines, the knockdown of METTL3 significantly increased the sensitivity to gemcitabine treatment and led to less colony formation. H In both Panc-1 and GEM-resistant Panc-1 cell lines, the knockdown of METTL3 significantly increased the sensitivity to gemcitabine treatment and led to less EDU incorporation. I In both Panc-1 and GEM-resistant Panc-1 cell lines, the knockdown of METTL3 significantly increased the sensitivity to gemcitabine treatment and led to more cell apoptosis.