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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. 2 — Exosomal ACADM predicted gemcitabine sensitivity of pancreatic cancer in vitro and in vivo. (A) CCK-8 assays indicated the cell growth of cells transfected with each siRNA. (B) The ACADM level in PC cells and its exosomes were detected by WB. (C) The ACADM level of each PC cell line was detected by WB. (D) IC50 values calculated from dose-response curves of high and low ACADM groups. (E) The ACADM level of PC cell-derived exosomes was detected by WB. (F) IC50 values calculated from dose-response curves of high and low exo-ACADM groups. (G) Tumor weight of xenografts treated or not with gemcitabine. (H) Xenografts of each cell line (gemcitabine-treated or control). (I) Correlation analysis between differential multiples of tumor weight and exo-ACADM in blood after gemcitabine treatment