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. 2018 Oct 23;8:15606. doi: 10.1038/s41598-018-33868-z

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© The Author(s) 2018

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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Model summarizing the obtained data. Both CTTN SH3 and NTA domain positively regulate EV release in invadopodia-forming MDA-MB-231. FSCN1 stimulates EV release independent of its actin-bundling function. EVs are preferentially secreted at invadopodia (a), but we cannot rule out the existence of other MVB docking sites (b). EVs are enriched in invadopodial proteins and auto- or paracrine EV uptake presumably stimulates de novo invadopodia formation (c) or stimulates existing invadopodia lifetime and maturation (d). Finally, EV possess matrix-degradative capacity, likely mediated by MT1-MMP, as the EVs are enriched in the membrane-bound metalloproteinase. MMP-9 and MMP-2 are potentially secreted in an EV-independent way and the latter MMPs may be activated by MT1-MMP (e). The concerted action of all MMPs is responsible pericellular matrix degradation and contributes to the overall invasive behaviour of MDA-MB-231 breast cancer cells.