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. 2019 May 22;21:66. doi: 10.1186/s13058-019-1147-7

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© The Author(s). 2019

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 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.

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Fig. 3 — Anxa2 tyrosine phosphorylation is required for the invasiveness of drug-resistant breast cancer cells. a The expression of Anxa2 and its mutants, Anxa2^Y23A and Anxa2^Y23D, were effectively rescued in Anxa2-silenced MCF-7/ADR cells as verified by Western blot analysis using anti-Anxa2- or anti-GFP-specific antibodies. β-actin was used as a loading control. b The re-expression of Anxa2^WT and the phospho-mimicking Anxa2^Y23D mutant, not the phospho-deficient Anxa2 ^Y23A mutant, in Anxa2-silenced cells rescued the migration and invasion ability. The cell migration and invasion assays were performed by transwell assay. Data are shown as mean ± SD; n = 6; ****P < 0.0001 and ^nsP > 0.05 indicate no statistical significance. The statistical results are summarized in the following panel