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. 2021 May 10;11:9838. doi: 10.1038/s41598-021-89288-z

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© The Author(s) 2021

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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Mechanical strain decreases proliferation and increases drug resistance in breast cancer cells. (A) Images of Bax and Bcl-2 immunostaining for cyclic mechanical strains of 0–17.5% strain. Bar = 100 μm. (B) Relative expression of pro-apoptotic Bax to anti-apoptotic Bcl-2 protein expression. *p < 0.05 versus 0% strain (n = 10). (C) Relative gene expression of Bax to Bcl-2 after 24 h of mechanical strain (n = 10). (D) Response of MDA-MB-231 breast cancer cells to drug treatment with paclitaxel, doxorubicin, or 5-fluorouracil under 0%, 7.5%, or 15% mechanical strain (n = 8). *p < 0.05 versus static conditions. ^†p < 0.05 versus static conditions under no treatment and under static conditions with the pharmacological treatment with same concentration as the indicated group. (E) Western blotting for cells treated with 7.5% strain in combination with DMSO, asciminib (Asc; Abl1 inhibitor), radotinib (Rad; c-Abl1 inhibitor), AZD1480 (Azd; Jak2 inhibitor), Ruxolitinib (Rux; Jak1/2 inhibitor), or a PI3K inhibitor (PI3K). (F) Western blotting for cells treated with 7.5% strain and the indicated inhibitors. Full-length blots/gels are presented in Supplemental Figs. S6–S7.