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. 2017 Jun 14;7:3486. doi: 10.1038/s41598-017-02358-z

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© The Author(s) 2017

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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Glucocorticoids mediate migratory and invasive properties stimulated by TGF-β1 in A549 cells. Cells were pretreated with or without dexamethasone (Dex, 2.5 μM) and fluticasone propionate (FP, 2.5 μM) for 1 hour and then stimulated with TGF-β1 (5 ng/ml). (A) Wound scratch and (B) Transwell migration assays established migration and invasion by A549 cells. Representative images are shown. In the wound scratching assays, the graphic representation is the percent of migrated cells counted within the areas of healing covering the lines present at baseline. In the Transwell migration assays, invasive cells were counted in five high-power fields (HPFs) for the average cell number migrated per HPF. (C) Visualization of F-actin used phalloidin with DAPI staining. Immunofluorescence was determined by confocal laser scanning microscope. Scale bar = 20 μm. Data are presented as means ± SEM. Results were from at least three independent experiments. *p < 0.05 vs. control; ^†p < 0.05 vs. TGF-β1.