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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. 1 — Distinct exosomal gene expression profiles in pancreatic cancer cells with different sensitivity [17]. (A) Median inhibitory dose of gemcitabine in different PC cells (IC50). (B) Cell viability of PC cells under 40 μm of gemcitabine. (C) Nanoparticle concentration of exosomes from pancreatic cancer cells detected by NTA. (D) The total amount of exosomes in pancreatic cancer cells was detected by WB. (E and F) KEGG pathway analysis of mass spectrometry results of exosomes proteins between sensitive and insensitive PC cells. (G) The volcano map reflects genes difference between sensitive and insensitive pancreatic cancer cells. (H) KEGG pathway analysis of RNA-seq results between sensitive and insensitive PC cells. (I) Wayne diagram shows the intersection of differential molecules of PC-derived exosomes and PC cells