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. 2021 May 21;12:297. doi: 10.1186/s13287-021-02378-7

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© The Author(s) 2021

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 — MSCs role in tumor metastasis (a) and angiogenesis (b). a The cancer cells release CXCL16 which can elicit the recruitment of MSCs in the tumor site. Upon the bindings of CXCL16 to CXCR6 on MSCs, they are transformed into CAFs producing high levels of CXCL12. CXCL12 stimulates the EMT process on cancer cells that promote CXCR4 expression in cancer cells, leading to their metastasis. b The MSCs commonly generate and release varied angiogenic mediators surrounding angiopoietin-1 (ANG-1) and IL-6 that, in turn, provoke the release of VEGF and other angiogenic factors stimulating tumor angiogenesis. CAF; cancer-associated fibroblast, EMT; epithelial-to-mesenchymal transition, MSC; mesenchymal stem/stromal cell, FGF; fibroblast growth factor, ANG-1; angiopoietin-1, PDGF; platelet-derived growth factor, VEGF; vascular endothelial growth factor