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. 2016 Sep 14;15:59. doi: 10.1186/s12943-016-0543-1

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© The Author(s). 2016

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 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.

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Fig. 9 — Proposed mechanism for ITSN-1s-mediated Eps8/Cbl/Sos1 interaction and Rac1-dependent LC cell migration and metastasis. ITSN-1s enhances Cbl-Eps8 interaction leading to ubiquitination and degradation of Eps8. The preferential formation of Cbl-Eps8 leads to impaired assembly of Sos1-Eps8, leading to deactivation of Rac1. Rac1 deactivation reorganizes the cytoskeleton structure to increase thick actin bundles, increase focal adhesion complexes and collapse of the vimentin filament network altogether leading to decreased LC cell migration and metastasis