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. 2021 Jun 26;21:320. doi: 10.1186/s12935-021-02022-7

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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. 5 — ARHGAP10 suppressed EMT in NSCLC cells by PI3K/Akt/GSK3β signaling. a Western blot detected the essential components of PI3K/Akt/GSK3β signaling pathway in A549 and NCI-H1299 cells. b Western blot was performed to explore EMT biomarkers expression in A549 and NCI-H1299 cells infected with ARHGAP10 virus or empty vector virus and treated with IGF-1 (100 ng/mL) for 24 h. c, d IGF-1 reversed the biological effects of ARHGAP10 on cell proliferation and invasion capabilities in A549 and NCI-H1299 cells. (*p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001)