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. 2020 Feb 18;10:2851. doi: 10.1038/s41598-020-59469-3

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© The Author(s) 2020

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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DHE mimics NR4A-dependent suppression of the MYC SE and displays similar efficacy to BET inhibitor JQ1. MOLM-14 cells were treated with 10 uM DHE or 500 nM JQ1 for 4 hours. (A) ChIP-qPCR for NR4A occupancy at the MYC SE in response to DHE treatment. (B) ChIP-qPCR for BRD4, MED1, CDK8, p300 and H3K27Ac. (C) ChIP-qPCR for total RNA polymerase II (Pol 2), Pol 2 phospho serine 5 (p-S5), Pol 2 phospho serine 2 (p-S2), and CDK9. ChIP-qPCRs for (A–C) were done using primer pairs specific for the MYC SE E1-E5 enhancers. NT represents a non-transcribed gene desert negative control. (D) RT-qPCR for enhancer RNAs (eRNAs) from the MYC SE E1-E5 as well as MYC mRNA in MOLM-14 cells. K562 cells are included as a negative control for eRNA expression at the MYC SE. (E) 3C chromatin looping frequency of interactions between the MYC SE E1-E5 and the MYC promoter. K562 cells are included as a non-looping negative control. Also included is a non-looping negative control genomic region between the MYC locus and the MYC SE. ***p < 0.001, **p < 0.01, *p < 0.05 compared to vehicle or K562 controls.