Differential modulation of the androgen receptor for prostate cancer therapy depends on the DNA response element.

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Abstrakt

Tytuł:: Differential modulation of the androgen receptor for prostate cancer therapy depends on the DNA response element.
Autorzy:: Kregel S; Michigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI 48109, USA.; Department of Pathology, University of Michigan, Ann Arbor, MI 48109, USA.
Bagamasbad P; Department of Human Genetics, University of Michigan, Ann Arbor, MI 48109, USA.
He S; Department of Human Genetics, University of Michigan, Ann Arbor, MI 48109, USA.
LaPensee E; Department of Human Genetics, University of Michigan, Ann Arbor, MI 48109, USA.
Raji Y; Department of Human Genetics, University of Michigan, Ann Arbor, MI 48109, USA.
Brogley M; Department of Human Genetics, University of Michigan, Ann Arbor, MI 48109, USA.
Chinnaiyan A; Michigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI 48109, USA.; Department of Pathology, University of Michigan, Ann Arbor, MI 48109, USA.; Department of Medicine and Urology, University of Michigan, Ann Arbor, MI 48109, USA.; Howard Hughes Medical Institute, University of Michigan, Ann Arbor, MI 48109, USA.; Rogel Cancer Center, University of Michigan, Ann Arbor, MI 48109, USA.
Cieslik M; Michigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI 48109, USA.; Department of Pathology, University of Michigan, Ann Arbor, MI 48109, USA.; Bioinformatics, University of Michigan, Ann Arbor, MI 48109, USA.
Robins DM; Department of Human Genetics, University of Michigan, Ann Arbor, MI 48109, USA.
Źródło:: Nucleic acids research [Nucleic Acids Res] 2020 May 21; Vol. 48 (9), pp. 4741-4755.
Typ publikacji:: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
Język:: English
Imprint Name(s):: Publication: 1992- : Oxford : Oxford University Press
Original Publication: London, Information Retrieval ltd.
MeSH Terms:: Response Elements*
Antibiotics, Antineoplastic/*pharmacology
Doxorubicin/*pharmacology
Gene Expression Regulation, Neoplastic/*drug effects
Prostatic Neoplasms/*genetics
Receptors, Androgen/*metabolism
Animals ; Antibiotics, Antineoplastic/therapeutic use ; Cell Line, Tumor ; Chromatin/drug effects ; Chromatin/metabolism ; Doxorubicin/therapeutic use ; HeLa Cells ; High-Throughput Screening Assays ; Humans ; Male ; Mice, SCID ; Prostatic Neoplasms/drug therapy ; Prostatic Neoplasms/metabolism ; RNA-Seq ; Xenograft Model Antitumor Assays
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Grant Information:: P30 DK020572 United States DK NIDDK NIH HHS; P50 CA186786 United States CA NCI NIH HHS; R35 CA231996 United States CA NCI NIH HHS; United States HHMI Howard Hughes Medical Institute
Substance Nomenclature:: 0 (Antibiotics, Antineoplastic)
0 (Chromatin)
0 (Receptors, Androgen)
80168379AG (Doxorubicin)
Entry Date(s):: Date Created: 20200322 Date Completed: 20200908 Latest Revision: 20200908
Update Code:: 20240105
PubMed Central ID:: PMC7229860
DOI:: 10.1093/nar/gkaa178
PMID:: 32198885
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Androgen receptor (AR) action is a hallmark of prostate cancer (PCa) with androgen deprivation being standard therapy. Yet, resistance arises and aberrant AR signaling promotes disease. We sought compounds that inhibited genes driving cancer but not normal growth and hypothesized that genes with consensus androgen response elements (cAREs) drive proliferation but genes with selective elements (sAREs) promote differentiation. In a high-throughput promoter-dependent drug screen, doxorubicin (dox) exhibited this ability, acting on DNA rather than AR. This dox effect was observed at low doses for multiple AR target genes in multiple PCa cell lines and also occurred in vivo. Transcriptomic analyses revealed that low dox downregulated cell cycle genes while high dox upregulated DNA damage response genes. In chromatin immunoprecipitation (ChIP) assays with low dox, AR binding to sARE-containing enhancers increased, whereas AR was lost from cAREs. Further, ChIP-seq analysis revealed a subset of genes for which AR binding in low dox increased at pre-existing sites that included sites for prostate-specific factors such as FOXA1. AR dependence on cofactors at sAREs may be the basis for differential modulation by dox that preserves expression of genes for survival but not cancer progression. Repurposing of dox may provide unique opportunities for PCa treatment.
(© The Author(s) 2020. Published by Oxford University Press on behalf of Nucleic Acids Research.)

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