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. 2017 Jul 18;7:5690. doi: 10.1038/s41598-017-05836-6

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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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Effect of AMPK agonist, AICAR, on TGF-β-induced EMT and Alteration of Intracellular Signaling Pathways. AICAR (5-amino-1-β-D-ribofuranosyl-imidazole-4-carboxamide, 10 μM) alleviates TGF-β1-induced changes in cell morphology (A) and the expression of E-cadherin and α-SMA (B). AICAR does not block an activation of Smad2/3 pathway (30 minutes) and MAPK phosphorylation (3 hours) (C). Representative cell morphology (A) and western blotting with quantitation graph are shown (B–D). N = 6. *p < 0.05 vs. others, ^#p < 0.05 vs. TGF-β1.