Cited by 317Prostate Cancer Treatment and ResearchChromatin Remodeling and CancerGenomics and Chromatin Dynamics

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A Somatically Acquired Enhancer of the Androgen Receptor Is a Noncoding Driver in Advanced Prostate Cancer

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Takeda, David Y., Spisák, Sándor, Seo, Ji-Heui, Bell, Connor, O’Connor, Edward, Korthauer, Keegan, Ribli, Dezső, Csabai, István, Solymosi, Norbert, Szállási, Zoltán, Stillman, David R., Cejas, Paloma, Qiu, Xintao, Long, Henry W., Tisza, Viktória, Nuzzo, Pier Vitale, Rohanizadegan, Mersedeh, Pomerantz, Mark M., Hahn, William C., Freedman, Matthew L.·2018·Cell

DOI 10.1016/j.cell.2018.05.037PMC PMC6046260

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Abstract

Increased androgen receptor (AR) activity drives therapeutic resistance in advanced prostate cancer. The most common resistance mechanism is amplification of this locus presumably targeting the AR gene. Here, we identify and characterize a somatically acquired AR enhancer located 650 kb centromeric to the AR. Systematic perturbation of this enhancer using genome editing decreased proliferation by suppressing AR levels. Insertion of an additional copy of this region sufficed to increase proliferation under low androgen conditions and to decrease sensitivity to enzalutamide. Epigenetic data generated in localized prostate tumors and benign specimens support the notion that this region is a developmental enhancer. Collectively, these observations underscore the importance of epigenomic profiling in primary specimens and the value of deploying genome editing to functionally characterize noncoding elements. More broadly, this work identifies a therapeutic vulnerability for targeting the AR and emphasizes the importance of regulatory elements as highly recurrent oncogenic drivers.

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Authors: Takeda, D. Y., Spisák, S., Seo, J.-H., Bell, C., O’Connor, E., Korthauer, K., Ribli, D., Csabai, I., Solymosi, N., Szállási, Z., Stillman, D. R., Cejas, P., Qiu, X., Long, H. W., Tisza, V., Nuzzo, P. V., Rohanizadegan, M., Pomerantz, M. M., Hahn, W. C., & Freedman, M. L.
Affiliations: Broad Institute (US)
Dana-Farber Cancer Institute (US)
Harvard University (US)
Eötvös Loránd University (HU)
University of Veterinary Medicine (HU)
Semmelweis University (HU)
Boston Children's Hospital (US)
Corresponding author: Freedman, Matthew L.
ORCID: Takeda, David Y.
Spisák, Sándor
Seo, Ji-Heui
Bell, Connor
O’Connor, Edward
Korthauer, Keegan
Ribli, Dezső
Csabai, István
Solymosi, Norbert
Szállási, Zoltán
Cejas, Paloma
Qiu, Xintao
Long, Henry W.
Tisza, Viktória
Nuzzo, Pier Vitale
Rohanizadegan, Mersedeh
Pomerantz, Mark M.
Hahn, William C.
Freedman, Matthew L.
Venue: Cell
Publisher: Elsevier BV
Published: 2018-07
Volume: 174
Issue: 2
Pages: 422-432.e13
ISSN: 0092-8674 (ISSN-L)
DOI: 10.1016/j.cell.2018.05.037
PMC: PMC6046260
OpenAlex: W2808687910
Cited by: 317
References: 55
Citations by year: 2026: 14 · 2025: 31 · 2024: 44 · 2023: 47 · 2022: 41 · 2021: 54 · 2020: 44 · 2019: 32 · 2018: 10
FWCI: 26.37
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 376 d)
Locations: Cell (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: Prostate Cancer Foundation Challenge Award
NIH (R01GM107427, R01CA193910, K08CA218530, R01HG005220, U01 CA176058)
National Research, Development and Innovation Fund of Hungary Project (FIEK_16-1-2016-0005)
Novo Nordisk Foundation Interdisciplinary Synergy Programme (NNF15OC0016584)
European Social Fund (EFOP-3.6.3-VEKOP-16-2017-00005)
Breast Cancer Research Foundation (BCRF-17-156)
H.L. Snyder Medical Research Foundation
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Prostate Cancer Treatment and Research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
Keywords: androgen receptor, advanced prostate cancer, treatment resistance, enzalutamide resistance, non-coding regulatory elements, genome editing, epigenetic profiling, oncogenic drivers
MeSH terms: Gene Editing, Acetylation, Adult, Aged, Antineoplastic Agents, Benzamides, Cell Survival, Enhancer Elements, Genetic, Histones, Humans, Male, Middle Aged, Neoplasm Metastasis, Nitriles, Phenylthiohydantoin, Receptors, Androgen, DNA Methylation, Cell Line, Tumor, CRISPR-Cas Systems, Prostatic Neoplasms, Castration-Resistant

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A Somatically Acquired Enhancer of the Androgen Receptor Is a Noncoding Driver in Advanced Prostate Cancer

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