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. 2023 Sep 28;23:221. doi: 10.1186/s12935-023-02997-5

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© The Author(s) 2023

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/. 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 in a credit line to the data.

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Fig. 8 — SQLE increases tumor cell migration and invasion by regulating the PTEN/AKT/GSK3β signaling pathway through P53. (A–C) The wound-healing assay demonstrated the capacity of migration in two BCa cells T24 and 5637; (D, E) The migration of T24 and 5637 cells were rescued by upregulation of P53 as measured by a transwell assay; Data represent the mean ± SD of three independent experiments. (*p < 0.05, **p < 0.01, ***p < 0.001, ns, not significant)