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. 2017 Sep 6;7:10662. doi: 10.1038/s41598-017-11106-2

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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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NR2E3 modulates AHR expression and responsiveness in cells. (a,b) MCF-7 and HepG2 cells were transfected with lentiviral-based small hairpin RNA (shRNA) targeting NR2E3 [shNR2E3 KO I & II] or a nonspecific control shRNA [shCT]. Effect of NR2E3 depletion on AHR and NR2E3 protein expressions and mRNA levels were detected by immunoblotting and qRT-PCR analysis. (c) Effect of NR2E3 depletion on the levels of CYP1A1 mRNAs induced by TCDD treatment (10 nM) in MCF-7 and HepG2 cells. (d,e) Effect of NR2E3 overexpression on AHR protein and mRNA levels in MCF-7 and HepG2 cells. (f) Effect of NR2E3 overexpression on the activity of reporter luciferase linked to consensus dioxin response element (DRE) in MCF-7 and HepG2 cells treated with and without TCDD treatment. Empty plasmid (Empty, pcDNA 4.0) was used as negative control. Results are means ± SE for at least two or three independent experiments with three replicates per experiment, and significantly (P < 0.05) increased (*) or reduced (**) responses are indicated.