ArticleNucleic acids research2020
Differential modulation of the androgen receptor for prostate cancer therapy depends on the DNA response element.
Article in Nucleic acids research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 32 citations in OpenAlex.
- A non-enzymatic role for METTL3 as an Androgen Receptor co-regulator that promotes prostate cancer proliferation.bioRxiv : the preprint server for biology · 2026Article
- Cardiac PTN-SIRT1 axis alleviates oxidative stress and promotes mitochondrial energy reprogramming to mitigate doxorubicin-induced cardiotoxicity through AMPK/PGC1α signaling.Acta biochimica et biophysica Sinica · 2026Article
- Evolving roles for the androgen receptor and its protein interactome in castration-resistant prostate cancer.Oncogene · 2025Review
- Androgen receptor-mediated assisted loading of the glucocorticoid receptor modulates transcriptional responses in prostate cancer cells.Genome research · 2025Article
- SOX2 utilizes FOXA1 as a heteromeric transcriptional partner to drive proliferation in therapy-resistant prostate cancer.bioRxiv : the preprint server for biology · 2025Article
- The Homeobox Transcription Factor NKX3.1 Displays an Oncogenic Role in Castration-Resistant Prostate Cancer Cells.Cancers · 2025Article
- Clinically Relevant Humanized Mouse Models of Metastatic Prostate Cancer Facilitate Therapeutic Evaluation.Molecular cancer research : MCR · 2024Article
- Androgen drives melanoma invasiveness and metastatic spread by inducing tumorigenic fucosylation.Nature communications · 2024Article
- Gastrodin inhibits prostate cancer proliferation by targeting canonical Wnt/β-catenin signaling pathway.Medical oncology (Northwood, London, England) · 2023Article
- TBC1D15 deficiency protects against doxorubicin cardiotoxicityActa pharmaceutica Sinica. B · 2023Article
- International Union of Basic and Clinical Pharmacology CXIII: Nuclear Receptor Superfamily-Update 2023.Pharmacological reviews · 2023Review
- Clinically relevant humanized mouse models of metastatic prostate cancer to evaluate cancer therapies.bioRxiv : the preprint server for biology · 2023Article
- Polydopamine-coated i-motif DNA/Gold nanoplatforms for synergistic photothermal-chemotherapy.Asian journal of pharmaceutical sciences · 2023Article
- Salidroside suppresses proliferation and migration in prostate cancer via the PI3K/AKT pathway.Cancer biomarkers : section A of Disease markers · 2023Article
- Self-assembly of DNA nanostructure containing cell-specific aptamer as a precise drug delivery system for cancer therapy in non-small cell lung cancer.Journal of nanobiotechnology · 2022Article
- The androgen receptor is a therapeutic target in desmoplastic small round cell sarcoma.Nature communications · 2022Article
- The relationship between sexual dimorphism and androgen response element proliferation in primate genomes.Evolution; international journal of organic evolution · 2022Article
- Biological roles and clinical significance of estrogen and androgen receptors in head and neck cancers.Journal of Cancer · 2022Review
- MET inhibition enhances PARP inhibitor efficacy in castration-resistant prostate cancer by suppressing the ATM/ATR and PI3K/AKT pathways.Journal of cellular and molecular medicine · 2021Article
- Somatic Alterations Impact AR Transcriptional Activity and Efficacy of AR-Targeting Therapies in Prostate Cancer.Cancers · 2021Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.