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. 2017 Oct 30;37(8):1049–1061. doi: 10.1038/onc.2017.403

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Copyright © 2018 The Author(s)

This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/4.0/

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Schematic of SPARCL1 suppresses OS metastasis and recruits macrophages by activation of canonical WNT/β-catenin signaling through stabilization of WNT–receptor complex. Once SPARCL1 is involved, it stabilizes canonical WNT ligand–receptor complex through physical interaction with FZDs and LRP5/6. Model 1, SPARCL1 bridges the FZDs and LRP5/6 proteins through a complex formation. Model 2, SPARCL1 may interact with both FZDs and LRP5/6, respectively, but not form a complex. In the presence of SPARCL1, enhanced WNT/β-catenin signaling directly inhibits OS metastasis. Additionally, SPARCL1-mediated activation of WNT/β-catenin signaling promotes macrophages recruitment to the osteosarcoma microenvironment by increasing CCL5 production in human OS cells.