ArticleProceedings of the National Academy of Sciences of the United States of America2022
H3K9 methylation drives resistance to androgen receptor-antagonist therapy in prostate cancer.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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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
32 citing papers in PubMed, 48 citations in OpenAlex.
- Striking the right balance with type I interferon signalling in cancer.Nature reviews. Cancer · 2026Review
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- Differential genetic analysis of ectrodactyly in a Fanconi anemia pedigree with FANCA mutations.MedScience · 2026Article
- Expression of endogenous retroviral elements is associated with extracellular matrix remodeling in prostate cancer.Mobile DNA · 2026Article
- Drug resistance in cancer: molecular mechanisms and emerging treatment strategies.Molecular biomedicine · 2025Review
- KDM3A drives NSCLC proliferation and metastasis via H3K9 demethylation, EMT activation and MMP-9 upregulation.Biomolecules & biomedicine · 2025Article
- The synergistic action of HDAC inhibitor with cisplatin impedes survival and proliferation of drug-tolerant persister in gastric and liver cancer cells.Clinical epigenetics · 2025Article
- Prostate cancer epigenetics - from pathophysiology to clinical application.Nature reviews. Urology · 2025Review
- NNMT promotes acquired EGFR-TKI resistance by forming EGR1 and lactate-mediated double positive feedback loops in non-small cell lung cancer.Molecular cancer · 2025Article
- Androgen Receptor Inhibition Increases MHC Class I Expression and Improves Immune Response in Prostate Cancer.Cancer discovery · 2025Article
- Epigenetic insights into prostate cancer: exploring histone modifications and their therapeutic implications.Frontiers in oncology · 2025Review
- Histone-modifying enzymes as drivers and therapeutic targets in androgen-resistant prostate cancer.Frontiers in endocrinology · 2025Review
- KDM3A Ablation Activates Endogenous Retrovirus Expression to Stimulate Antitumor Immunity in Gastric Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Review
- Insights into immune microenvironment and therapeutic targeting in androgen-associated prostate cancer subtypes.Scientific reports · 2024Article
- Review
- GZ17-6.02 kills PDX isolates of uveal melanoma.Oncotarget · 2024Article
- Chronic hypoxia stabilizes 3βHSD1 via autophagy suppression.Cell reports · 2024Article
- Histone methyltransferase SUV39H2 regulates apoptosis and chemosensitivity in prostate cancer through AKT/FOXO signaling pathway.Medical oncology (Northwood, London, England) · 2024Article
- Review
Corrections and comments
- Commented on byUro-Science.2023
Authors and funding
17 authors at 5 institutions in 3 countries.
Funding
Abstract
Antiandrogen strategies remain the prostate cancer treatment backbone, but drug resistance develops. We show that androgen blockade in prostate cancer leads to derepression of retroelements (REs) followed by a double-stranded RNA (dsRNA)-stimulated interferon response that blocks tumor growth. A forward genetic approach identified H3K9 trimethylation (H3K9me3) as an essential epigenetic adaptation to antiandrogens, which enabled transcriptional silencing of REs that otherwise stimulate interferon signaling and glucocorticoid receptor expression. Elevated expression of terminal H3K9me3 writers was associated with poor patient hormonal therapy outcomes. Forced expression of H3K9me3 writers conferred resistance, whereas inhibiting H3K9-trimethylation writers and readers restored RE expression, blocking antiandrogen resistance. Our work reveals a drug resistance axis that integrates multiple cellular signaling elements and identifies potential pharmacologic vulnerabilities.
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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.