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. 2017 Aug 15;7:8136. doi: 10.1038/s41598-017-08225-1

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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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Atranorin suppressed KITENIN-mediated AP-1 activity, affected the expression of KAI1 and KITENIN, and downregulated c-jun and c-fos. (a) Atranorin inhibited the KITENIN-mediated transcriptional activity of the AP-1 promoter. After 12 h of transfection with KITENIN and the AP-1 reporter plasmid, cells were treated with atranorin for 48 h in the presence or absence of EGF. (b) Western blot analysis of total, cytoplasmic, and nuclear c-jun, phospho-c-jun (ser63), and c-fos in A549 cells. (c) Western blot analysis of KITENIN in A549 cells treated with 5 μg/mL atranorin. (d) Quantitative analysis of the mRNA level of KITENIN and KAI1 in A549 cells treated with different concentrations of atranorin. (e,f) KITENIN 3′-UTR (e) and promoter (f) luciferase assays in HEK293T cells treated with atranorin. Quantitative data were obtained from at least two independent experiments. Data represent the mean ± S.E.M. (n = 3). *p < 0.05; **p < 0.01; ***p < 0.001; NS, no significant difference compared with the DMSO-treated group in each cell line.