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. 2023 Aug 23;23:789. doi: 10.1186/s12885-023-11239-w

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© The Author(s) 2023

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 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. 4 — ACADM regulated chemosensitivity via fatty acid degradation in pancreatic cancer cells. (A)Activity of pancreatic cancer cells under gemcitabine IC50 concentration (ACADM knockdown or overexpression). (B) Xenografts of each cell line (ACADM knockdown or control group) treated with gemcitabine. (C)Tumor weight of xenografts treated with gemcitabine. (D)The total fatty acid level in PC cells and its relationship with exo-ACADM level. (E) The Acetyl-CoA level in PC cells and its relationship with exo-ACADM level. (F)The total fatty acid level in PC cells after transfection of ACADM knockdown or overexpression plasmid. (G)The Acetyl-CoA level in PC cells after transfection of ACADM knockdown or overexpression plasmid. (H) Heatmap showing the level of medium and long-chain fatty acids after ACADM knockdown