ArticleNature chemical biology2016
Inhibiting androgen receptor nuclear entry in castration-resistant prostate cancer.
Article in Nature chemical biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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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
16 citing papers in PubMed, 22 citations in OpenAlex.
- Profiling crystal engineered ligands for targeting treatment resistant androgen receptors.bioRxiv : the preprint server for biology · 2026Article
- Androgen Receptor Point Mutations: A Mechanism of Therapeutic Resistance and a Framework for Rational Drug Design.Cancers · 2026Review
- Targeting Androgen Receptor as a Novel Radiosensitizing Therapy to Improve Long-Term Survival and Anti-tumor Immunity in Glioblastoma via TGF-β/Smad3 Axis Reprogramming.Research square · 2026Article
- Profiling crystal engineered ligands for targeting treatment resistant androgen receptors.Frontiers in pharmacology · 2026Article
- ADT increases prostate cancer cell invasion via altering AR/SALL4/SOX2-OCT4 stem cell signaling.Cell biology and toxicology · 2025Article
- Molecular pathways in reproductive cancers: a focus on prostate and ovarian cancer.Cancer cell international · 2025Review
- Small-molecule disruption of androgen receptor-dependent chromatin clusters.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Article
- An overview of PROTACs: a promising drug discovery paradigm.Molecular biomedicine · 2022Review
- Yeast-based evolutionary modeling of androgen receptor mutations and natural selection.PLoS genetics · 2022Article
- In Vitro characterization of the endocrine disrupting effects of per- and poly-fluoroalkyl substances (PFASs) on the human androgen receptor.Journal of hazardous materials · 2022Article
- Androgen Receptor, Although Not a Specific Marker For, Is a Novel Target to Suppress Glioma Stem Cells as a Therapeutic Strategy for Glioblastoma.Frontiers in oncology · 2021Article
- Therapeutic targeting of the androgen receptor (AR) and AR variants in prostate cancer.Asian journal of urology · 2020Review
- Androgen Receptor Is a Non-canonical Inhibitor of Wild-Type and Mutant Estrogen Receptors in Hormone Receptor-Positive Breast Cancers.iScience · 2019Article
- Recent advances on the progressive mechanism and therapy in castration-resistant prostate cancer.OncoTargets and therapy · 2018Review
- Androgen receptor antagonism drives cytochrome P450 17A1 inhibitor efficacy in prostate cancer.The Journal of clinical investigation · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 3 institutions in 1 country.
Funding
Abstract
Clinical resistance to the second-generation antiandrogen enzalutamide in castration-resistant prostate cancer (CRPC), despite persistent androgen receptor (AR) activity in tumors, highlights an unmet medical need for next-generation antagonists. We have identified and characterized tetra-aryl cyclobutanes (CBs) as a new class of competitive AR antagonists that exhibit a unique mechanism of action. These CBs are structurally distinct from current antiandrogens (hydroxyflutamide, bicalutamide, and enzalutamide) and inhibit AR-mediated gene expression, cell proliferation, and tumor growth in several models of CRPC. Conformational profiling revealed that CBs stabilize an AR conformation resembling an unliganded receptor. Using a variety of techniques, it was determined that the AR-CB complex was not recruited to AR-regulated promoters and, like apo AR, remains sequestered in the cytoplasm, bound to heat shock proteins. Thus, we have identified third-generation AR antagonists whose unique mechanism of action suggests that they may have therapeutic potential in CRPC.
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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.