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. 2020 Sep 18;12(1):29–38. doi: 10.1007/s13238-020-00786-8

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© The Author(s) 2020

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/.

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Schematic of FOXA1 activity in (A) normal prostate and (B) prostate cancer. (A) FOXA1 preferentially binds to genomic Forkhead motifs marked by H3K4me1/me2 histone modifications. It induces open chromatin conformation and allows for the sequential binding of AR to drive AR transcriptional programs. FOXA1 also inhibits EMT independent of AR. (B) In prostate cancer, FOXA1 can extensively reprogram AR cistrome along with HOXB13. FOXA1 mutations can result in stronger AR binding and significantly alter AR transcriptional programs. FOXA1 mutants can also induce EMT programs to drive cancer metastasis. Abbreviations: ARE, androgen-receptor response element; EMT, epithelial-mesenchymal transition