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. 2021 Mar 9;11:5457. doi: 10.1038/s41598-021-84769-7

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© The Author(s) 2021

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 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/.

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Effect of cyproterone acetate (CPA) on the transactivation activity of the aryl hydrocarbon response element (AHRE) in human cells. Reporter plasmids, (a,b) pTAL-Luc and RSV-lacZ or (c-h) pAhRDtkLuc3 and RSV-lacZ, were transient transfected into HepG2 and MCF7 cells for 18 h, and then cells were treated with the test compounds. (a) HepG2 cells were treated with CPA (10 μM) for 2–10 h. (b) HepG2 cells were treated with CPA (1–30 μM) for 6 h. (c,d) HepG2 and MCF7 cells were treated with CPA (10 μM) for 2–10 h. (e,f) HepG2 and MCF7 cells were treated with CPA (1–30 μM) for 6 h. (g,h) HepG2 cells were pretreated 0.5–30 μM CPA for 1 h, followed by treatment with 0.5 μM ITE for 6 h and 0.5 μM β-NF for 9 h respectively. At the end of incubation with the test compounds, cells were harvested and cell lysates were collected for an activity assay of luciferase and β-galactosidase. Results are expressed as the mean ± SD, n = 3. **p < 0.01, and ***p < 0.001.