ArticleeLife2017
A comprehensive analysis of coregulator recruitment, androgen receptor function and gene expression in prostate cancer.
Article in eLife, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 55 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
55 citing papers in PubMed, 76 citations in OpenAlex.
- Targeting the Androgen Receptor and Associated Cofactors in Prostate Cancer: Novel Approaches and Future Perspectives.International journal of molecular sciences · 2026Review
- Multi-omics dissection of FOXA1 reveals cancer-type-specific transcriptional networks and functional risk variants.iScience · 2026Article
- Androgens protect ILC2S from functional suppression during influenza virus infection.Mucosal immunology · 2026Article
- Decoding the germline genetic architecture of prostate cancer at a single cell resolution.PLoS genetics · 2025Article
- Overexpression of androgen receptor signalling transactivator lncRNAs PRNCR1 and PCGEM1 are associated with the increased risk of PCOS.Scientific reports · 2025Article
- Evolving roles for the androgen receptor and its protein interactome in castration-resistant prostate cancer.Oncogene · 2025Review
- Disrupting the interaction between androgen receptor and its coregulator WDR77 delays the growth of treatment-resistant prostate cancer.Cell reports · 2025Article
- Genomic features of the methylosome protein MEP50 and its implications in hormone signaling and cancer.Endocrine connections · 2025Article
- Cutting edge: Extrinsic and intrinsic sex effects differentially regulate pulmonary ILC2 numbers, phenotype, and function.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- The Role of WDR77 in Cancer: More than a PRMT5 Interactor.Molecular cancer research : MCR · 2025Review
- Reduction of Prostate Cancer Risk: Role of Frequent Ejaculation-Associated Mechanisms.Cancers · 2025Review
- The Homeobox Transcription Factor NKX3.1 Displays an Oncogenic Role in Castration-Resistant Prostate Cancer Cells.Cancers · 2025Article
- Context-specific targeting of the androgen receptor in prostate cancer.Nature genetics · 2024Article
- Race-specific coregulatory and transcriptomic profiles associated with DNA methylation and androgen receptor in prostate cancer.Genome medicine · 2024Review
- Review
- Androgen Receptor-Interacting Proteins in Prostate Cancer Development and Therapy Resistance.The American journal of pathology · 2024Review
- Identification of Molecular Markers Associated with Prostate Cancer Subtypes: An Integrative Bioinformatics Approach.Biomolecules · 2024Article
- Androgen Receptor in Hormone Receptor-Positive Breast Cancer.International journal of molecular sciences · 2023Review
- Prostate Cancer Progression Relies on the Mitotic Kinase Citron Kinase.Cancer research · 2023Article
- International Union of Basic and Clinical Pharmacology CXIII: Nuclear Receptor Superfamily-Update 2023.Pharmacological reviews · 2023Review
Corrections and comments
- Erratum issued
Authors and funding
24 authors at 3 institutions in 2 countries.
Funding
Abstract
Standard treatment for metastatic prostate cancer (CaP) prevents ligand-activation of androgen receptor (AR). Despite initial remission, CaP progresses while relying on AR. AR transcriptional output controls CaP behavior and is an alternative therapeutic target, but its molecular regulation is poorly understood. Here, we show that action of activated AR partitions into fractions that are controlled preferentially by different coregulators. In a 452-AR-target gene panel, each of 18 clinically relevant coregulators mediates androgen-responsiveness of 0-57% genes and acts as a coactivator or corepressor in a gene-specific manner. Selectivity in coregulator-dependent AR action is reflected in differential AR binding site composition and involvement with CaP biology and progression. Isolation of a novel transcriptional mechanism in which WDR77 unites the actions of AR and p53, the major genomic drivers of lethal CaP, to control cell cycle progression provides proof-of-principle for treatment via selective interference with AR action by exploiting AR dependence on coregulators.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.