ArticleNature cell biology2021
An androgen receptor switch underlies lineage infidelity in treatment-resistant prostate cancer.
Article in Nature cell biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers.
What it found
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Who cites it
124 citing papers in PubMed, 157 citations in OpenAlex.
- Genes, fuel, and fate in lung cancer.Biochemical Society transactions · 2026Review
- Non-conventional histologies of prostate cancer: from morphology to biology-driven precision oncology.The oncologist · 2026Review
- Cell plasticity in cancer and therapy resistance.Experimental & molecular medicine · 2026Review
- Spatial and Epigenetic Polarity of the AR Promoter During Prostate Cancer Progression: An In Silico Analysis.International journal of molecular sciences · 2026Article
- Castration-resistant prostate cancer as an adaptive tumor ecosystem: coupling tumor evolution with microenvironmental reprogramming.Cancer metastasis reviews · 2026Review
- Targeting the Androgen Receptor and Associated Cofactors in Prostate Cancer: Novel Approaches and Future Perspectives.International journal of molecular sciences · 2026Review
- Castration-resistant prostate cancer cells are addicted to the high activity of cyclin-dependent kinase 2.Molecular oncology · 2026Article
- Histone modifications: mechanisms, metabolic regulation, and therapeutic targeting in cancer.Precision clinical medicine · 2026Review
- WSB1-Mediated PSMA Ubiquitination Promotes Enzalutamide-Induced Neuroendocrine-like Transition in Patient-Derived Prostate Cancer Spheroids.International journal of molecular sciences · 2026Article
- SETDB1-mediated repression of RhoB promotes EMT and metastatic progression in prostate cancer.Oncogene · 2026Article
- Towards implementation of precision medicine biomarkers in early detection and prognostication of prostate cancer.Cancer metastasis reviews · 2026Review
- Mapping prostate cancer pathobiology: A review of genetically engineered mouse models (GEMMs).Gene · 2026Review
- Therapeutic targeting of the eIF4E cap-binding domain reveals control of lineage fate in prostate cancer.The Journal of clinical investigation · 2026Article
- USP2 is an androgen-repressed survival factor that stabilises oncoproteins to facilitate therapy resistance in prostate cancer.Cell death & disease · 2026Article
- Molecular determinants of AR-enhancer interaction and cistrome reprogramming in prostate cancer progression.Endocrine-related cancer · 2026Review
- Review
- IGFBP3-SphK1/S1P Signaling Axis Drives Enzalutamide Resistance in Advanced Prostate Cancer.Molecular cancer therapeutics · 2026Article
- Review
- SMARCA4 promotes lineage plasticity and enzalutamide resistance in prostate cancer by regulating PROX1 via H3K27 acetylation.Cell death discovery · 2026Article
- UHRF1 regulates AR ubiquitination to promote the loss of AR signaling and enzalutamide resistance in progression of prostate cancer.Cell death & disease · 2026Article
64 more citing papers are in PubMed but not listed here.
Corrections and comments
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- Commented on byUro-Science.2022
Authors and funding
32 authors at 10 institutions in 5 countries.
Funding
Abstract
Cancers adapt to increasingly potent targeted therapies by reprogramming their phenotype. Here we investigated such a phenomenon in prostate cancer, in which tumours can escape epithelial lineage confinement and transition to a high-plasticity state as an adaptive response to potent androgen receptor (AR) antagonism. We found that AR activity can be maintained as tumours adopt alternative lineage identities, with changes in chromatin architecture guiding AR transcriptional rerouting. The epigenetic regulator enhancer of zeste homologue 2 (EZH2) co-occupies the reprogrammed AR cistrome to transcriptionally modulate stem cell and neuronal gene networks-granting privileges associated with both fates. This function of EZH2 was associated with T350 phosphorylation and establishment of a non-canonical polycomb subcomplex. Our study provides mechanistic insights into the plasticity of the lineage-infidelity state governed by AR reprogramming that enabled us to redirect cell fate by modulating EZH2 and AR, highlighting the clinical potential of reversing resistance phenotypes.
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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.