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. 2021 May 11;22:149. doi: 10.1186/s13059-021-02339-6

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© The Author(s) 2021

Open AccessThis 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/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 6 — SNVs impact AR enhancer activity. a An increase in SNVs at ARBS is observed in both primary (left) and metastatic (right) PCa. b The impact of clinical SNV on androgen-dependent enhancer activity was quantified with a luciferase assay at inducible ARBS. Those SNVs that significantly altered AR enhancer activity (3/16) are shown (4 biological replicates ± SEM; *p < 0.05, ***p < 0.001). c Genome browser snapshot of ZBTB16 gene locus. Gene looping is observed between enhancer ARBS_490 and ZBTB16 promoter. d Expression of ZBTB16 was quantified by qPCR after CRISPRi inhibition of ARBS_490. Androgen-induced expression of ZBTB16 is suppressed compared to non-target (NT) gRNA control (3 biological replicates ± SEM; **p < 0.01)