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. 2018 Nov 30;8:17477. doi: 10.1038/s41598-018-35392-6

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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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Pharmacological inhibition of cdc42 activity rescued MEC-17-induced suppression of EMT. (A) The representative Western blots show the protein levels of vimentin, MEC-17, and acetyl-α-tubulin in vector control and MEC-17-overexpressed A549 cells after treatment with TGFβ1 (20 ng/mL) for 48 h. Beta-actin served as the internal control. The relative vimentin intensities normalized to vector control group were shown. Uncropped blots are displayed in the supplementary information (Supplementary Fig. S5). (B) The representative Western blots show the protein levels of vimentin, MEC-17, and acetyl-α-tubulin in vector control or MEC-17-overexpressed A549 cells after treatment with the cdc42 inhibitor CASIN (5 μM) for 48 h. Beta-actin served as the internal control. The relative vimentin intensities normalized to vector control group were shown. Uncropped blots are displayed in the supplementary information (Supplementary Fig. S5).