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. 2022 Feb 23;12:774988. doi: 10.3389/fonc.2022.774988

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Copyright © 2022 Shao, Piao, Wang, Guo, Wang, Wang, Tong, Yuan, Han, Fang, Zhu and Wang

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Tspan9-β1 interactions promote FAK-Src-Ras-ERK1/2 pathway signaling and OS metastasis. (A) Interactions between Tspan9 and integrin β1 were detected in a co-IP assay. (B) FAK-Ras-ERK1/2 pathway proteins (FAK^Y397, total-FAK, Ras, pERK1/2, and total-ERK1/2) were analyzed via western blotting, with β-actin as a loading control. (C) Quantification of the Western blotting results presented in (B). (D) Western blotting was used to assess Ras downstream signaling in OE-Tspan9 U2OS cells following Salirasib treatment (50μM). (E) Following treatment with Salirasib (50μM), OE-Tspan9 cells were analyzed in migration and invasion assays, with representative cells being shown. (F) Schematic presentation of mechanism underlying Tspan9-mediated OS metastasisis. All analyzes were repeated two or three times. Data are means ± SD. *P < 0.05; **P < 0.01; ***P < 0.001.