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. 2022 Sep 29;41:289. doi: 10.1186/s13046-022-02483-2

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© The Author(s) 2022

Open AccessThis 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. 4 — FOXM1-PROTAC inhibits proliferation, migration and invasion of cancer cells. A Analysis for DNA content of HepG2 and MDA-MB-231 cells on a Flow cytometer, treated with FIP-1 and FOXM1-PROTAC for 24 h and stained with propidium iodide. B Scratch assay of HepG2 and MDA-MB-231 cells, which were treated with FIP-1 and FOXM1-PROTAC for 24 h. C Colony formation results and analysis of HepG2 and MDA-MB-231 cells, which were treated with FIP-1 and FOXM1-PROTAC for 24 h and cultured for 14 days. D Transwell experiment and Statistical histogram, which reflects different invasion ability of HepG2 and MDA-MB-231 cells treated with FIP-1 and FOXM1-PROTAC for 24 h. E Examination of E-cadherin, N-cadherin and Vimentin level of HepG2 and MDA-MB-231 cells, treated with FIP-1 and FOXM1-PROTAC for 48 h