SynthesisCancer research2023
Androgen Receptor Variants Confer Castration Resistance in Prostate Cancer by Counteracting Antiandrogen-Induced Ferroptosis.
Synthesis in Cancer research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.
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.
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Who cites it
44 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.
- A comprehensive bibliometric analysis of ferroptosis in tumor resistance: development and emerging trends.Frontiers in immunology · 2025Pooled it
- PABPC1 dictates castration sensitivity in prostate cancer via orchestrating ferroptosis resistance and CD8(+) T-cell dysfunction.Cell death and differentiation · 2026Article
- Article
- Ferroptosis at the Metabolic-Immune Interface in Metastatic Castration-Resistant Prostate Cancer: Mechanistic Evidence, Translational Gaps, and Combination Strategies.Annals of surgical oncology · 2026Review
- Ferroptosis and prostate cancer: A translational path from molecular mechanisms to precision therapy.Genes & diseases · 2026Review
- Proteomic Analysis Reveals AMPKα-Mediated Antiandrogen Resistance via Ferroptosis Suppression in Prostate Cancer.Cancer science · 2026Article
- Article
- Review
- Metabolic vulnerabilities in advanced prostate cancer: the interplay of ferroptosis, cuproptosis, and the inflammatory microenvironment.Medical oncology (Northwood, London, England) · 2026Review
- Virtual screening and experimental validation of small-molecule compounds targeting AR in prostate cancer.Molecular diversity · 2026Article
- DDX5 (p68) and UbE2T as emerging superior cancer therapeutic targets: dual molecular glue target degradation by FL118 for conquering difficult-to-treat cancers.Journal of experimental & clinical cancer research : CR · 2026Review
- Androgen receptor and fatty acid oxidation cooperate in ferroptosis evasion in BRAFi resistant melanoma.Cell death & disease · 2026Article
- KDM5B-driven glucose metabolic reprogramming promotes enzalutamide resistance in prostate cancer via the lactate/hnRNPA1 lactylation/AR-V7 axis.Molecular cancer · 2026Article
- PDHA1-acetylation signaling suppresses cuproptosis to attenuate anti-androgen effect in prostate cancer.Cell death & disease · 2026Article
- SOX8/CPT2 axis regulates lipid metabolism to support enzalutamide resistance in prostate cancer.Cancer cell international · 2026Article
- Targeting Hsp70 triggers ferroptosis: a novel anti-cancer mechanism of a marine natural product in prostate cancer.Natural products and bioprospecting · 2026Article
- Integrated regulation of ferroptosis in prostate cancer covering mechanisms, resistance, and translational opportunities.Journal of molecular medicine (Berlin, Germany) · 2026Review
- Transcriptional and epigenetic reprogramming, lineage plasticity and therapy resistance in prostate cancer.Journal of the National Cancer Center · 2026Review
- Hyperandrogenemia Induces Trophoblast Ferroptosis and Early Pregnancy Loss in Patients With PCOS via CMA-Dependent FTH1 Degradation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Reversing enhancer RNA-mediated IKBKE gene repression enables synthetic anticancer immunity in prostate cancer models.The Journal of clinical investigation · 2026Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Androgen receptor (AR) inhibition by androgen deprivation and/or antiandrogen administration is the mainstay therapy for advanced prostate cancer. However, most prostate cancers ultimately become resistant to these therapies, indicating the importance of identifying mechanisms driving resistance to improve patient outcomes. Here we demonstrated that acute treatment with the antiandrogen enzalutamide (ENZ) decreased glutathione (GSH) production, increased lipid peroxidation, and induced ferroptosis in prostate cancer cells. Consistently, meta-analysis of transcriptomic data linked the androgen-AR axis to metabolism-related biological processes, including lipid metabolism. The cystine transporter gene SLC7A11 was a key AR target, and full-length AR (AR-FL) transactivated SLC7A11 transcription by directly occupying the SLC7A11 promoter and putative enhancer regions. AR variants (AR-V) preferentially bound the SLC7A11 enhancer and upregulated SLC7A11 expression, thereby conferring resistance to ferroptosis induced by ENZ treatment. However, this effect was abolished following downregulation of AR-Vs using the dual CBP/p300 and BET inhibitor NEO2734. These findings reveal ferroptosis induction as an anticancer mechanism of antiandrogens and SLC7A11 as a direct target gene of AR-FL and AR-Vs. AR-V-mediated SLC7A11 expression represents a mechanism coupling ferroptosis resistance to prostate cancer progression. SIGNIFICANCE: Upregulation of SLC7A11 can be induced by androgen receptor variants to inhibit antiandrogen-induced prostate cancer cell ferroptosis and to drive castration resistance in prostate cancer.
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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.