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. 2024 Jun 22;15(6):440. doi: 10.1038/s41419-024-06822-3

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© The Author(s) 2024

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. 3 — a Inhibition of endocytosis by 40 µM fasudil significantly decreased the viability of U87, PC3, BT549, A549, HepG2 and SUM159 cancer cells treated with 400 ng/mL sFasL. b The viability of HUVECs, HBEs, and iPS-cardiomyocytes significantly decreased upon the same treatment, but this decrease was not as dramatic as that observed in cancer cells. c Caspase-3 and caspase-8 activity in U87 cells significantly increased upon a combination of sFasL treatment with fasudil. d Schematics describe the experiments where inhibition of endocytosis was limited to 30 min and caspase-8 activity was quantified after 24 h (upper panel). Chemical inhibition was attained by treating cells with either 5 µM dyngo-4a or 2 µM pitstop-2. Mechano-inhibition involved increasing the plasma membrane tension of cells via hypotonic swelling for 30 min in the presence of sFasL. After this point, the hypotonic medium was replaced with isotonic medium (containing sFasL) to cease mechano-inhibition of endocytosis (****p < 0.0001, ***p < 0.001, **p < 0.01; *p < 0.05; one-way ANOVA).