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. 2020 Dec 1;124(1):207–216. doi: 10.1038/s41416-020-01173-0

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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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — a Representative images of cell migration and wound repair; cells were allowed to migrate 8, 24, 32 and 48 h after wounding. b Representative images of cell invasion; cells were allowed to invade the Matrigel-coated transwell membrane for 24 and 48 h. c TUBO cell migration and wound repair capability was slower compared to 4T1 cells; data are shown as mean ± SD (n = 3). *P < 0.05; **P < 0.01. d TS/A cells were the most invasive cells after 24 and 48 h; data are shown as mean ± SD (n = 3). **P < 0.01. e–g Graphs showing the mean ± SD of Sca1⁺, CD44⁺CD24⁻ cells and CD44 mean fluorescence intensity (MFI) from three independent experiments. *P < 0.05; **P < 0.01; ***P < 0.001.