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. 2020 Aug 18;43(6):1161–1174. doi: 10.1007/s13402-020-00549-x

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© The Author(s) 2020

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/.

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Fig. 6 — Mesenchymal transition protects tumor cells from macrophage induced cytotoxicity. (A) MTT viability assays of PANC-1 shCtrl, shZEB1 #1 and shZEB1 #2 cells treated with RPMI-1640 (green bars) or M0-CM (blue bars). PAR1 was inhibited by Vorapaxar (500 nM), MMP9 was inhibited by GM6001 (5 μM), and DMSO served as a mock control. Decreased viability was calculated relative to the viability of control-treated cells. Shown is the mean ± SEM (n = 6); One-way ANOVA. (B) Schematic representation showing that macrophages secrete MMP9 that activates PAR1 on pancreatic cancer cells, thereby inducing mesenchymal transition and subsequent resistance to macrophage-induced cytotoxicity