ArticleNature genetics2024
NSD2 is a requisite subunit of the AR/FOXA1 neo-enhanceosome in promoting prostate tumorigenesis.
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Article in Nature genetics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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29 citing papers in PubMed.
- Targeting the Androgen Receptor and Associated Cofactors in Prostate Cancer: Novel Approaches and Future Perspectives.International journal of molecular sciences · 2026Review
- NSD Histone Methyltransferases in Solid Tumors: Biological Functions, Oncogenic Mechanisms and Therapeutic Targeting.International journal of molecular sciences · 2026Review
- Epigenetics in development, disease, and therapy: from mechanisms to clinical interventions.Science China. Life sciences · 2026Review
- A ligandable PNT domain establishes ERG as a directly targetable oncogenic driver in prostate cancer.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- NNMT Loss Drives Cancer Progression by enhancing SAM availability for mTORC1 Signaling and Chromatin Methylation.bioRxiv : the preprint server for biology · 2026Article
- Histone methyltransferase KMT2D promotes castration-resistant prostate cancer progression by reactivating AR through FOXA1.Oncogene · 2026Article
- Molecular determinants of AR-enhancer interaction and cistrome reprogramming in prostate cancer progression.Endocrine-related cancer · 2026Review
- MECOM Function Is Critical for AR-Driven Treatment-Resistant Prostate Cancer.Cancer research · 2026Article
- Rewiring Oncogenic Transcriptional Complexes with Domain-ALTeration Chimeras (DALTACs) in Prostate Cancer.bioRxiv : the preprint server for biology · 2026Article
- STAG2 loss amplifies EWS-FLI1-driven microsatellite enhancer activity promoting Ewing sarcoma aggressiveness.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Article
- FOXA1 mutations co-opt nascent transcription factor networks in partnership with androgen receptor to enhance prostate tumorigenicity.Cell reports · 2026Article
- Crosstalk between EZH2 and DNA methylation mediates neuroendocrine prostate cancer lineage plasticity.Nature communications · 2026Article
- Emerging therapies to overcome antiandrogen resistance and beyond in lethal prostate cancer.Journal of the National Cancer Center · 2026Review
- Alterations in AR-FOXA1 signaling in prostate cancer progression and therapeutic resistance.Journal of the National Cancer Center · 2026Review
- Article
- Systematic investigation of zinc finger MYND-type containing 11-mediated alternative splicing reveals notable events in prostate cancer.Asian journal of urology · 2026Article
- Article
- NSD Family-Mediated H3K36 Methylation in Human Cancer: Mechanisms and Therapeutic Opportunities.Biomedicines · 2025Review
- NSD2 mediates NF-κB and matrix metalloproteinases to drive hepatocellular carcinoma malignant progression.Translational cancer research · 2025Article
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Authors and funding
35 authors.
Abhijit ParoliaMichigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, USA. aparolia@umich.edu.ORCID http://orcid.org/0000-0003-0238-221X
Sanjana Eyunni *Michigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, USA.
Brijesh Kumar Verma *Department of Cancer Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Eleanor YoungMichigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, USA.ORCID http://orcid.org/0000-0001-5393-530X
Yihan LiuMichigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, USA.
Lianchao LiuState Key Laboratory of Chemical Biology, Shanghai Institute of Organic Chemistry, Chinese Academy of Sciences, Shanghai, China.
James GeorgeMichigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, USA.ORCID http://orcid.org/0000-0002-9723-6444
Shweta ArasDepartment of Cancer Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Chandan Kanta DasDepartment of Cancer Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Rahul MannanMichigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, USA.ORCID http://orcid.org/0000-0002-6642-0468
Reyaz Ur RasoolDepartment of Cancer Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Erick Mitchell-VelasquezDepartment of Cancer Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Somnath MahapatraMichigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, USA.ORCID http://orcid.org/0000-0001-9490-6353
Jie LuoMichigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, USA.
Sandra E CarsonMichigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, USA.ORCID http://orcid.org/0000-0002-7716-9627
Lanbo XiaoMichigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, USA.
Prathibha R GajjalaMichigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, USA.
Sharan VenkateshDepartment of Cancer Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Mustapha JaberMichigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, USA.ORCID http://orcid.org/0009-0003-1632-3154
Xiaoju WangMichigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, USA.
Tongchen HeMichigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, USA.
Yuanyuan QiaoMichigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, USA.ORCID http://orcid.org/0000-0002-1178-3480
Matthew PangMichigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, USA.
Yuping ZhangMichigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, USA.
Jean Ching-Yi TienMichigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, USA.
Micheala LouwDepartment of Pathology, University of Michigan, Ann Arbor, MI, USA.
Mohammed AlhusayanDepartment of Cancer Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Xuhong CaoMichigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, USA.
Fengyun SuMichigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, USA.
Omid TavanaBioscience, Research and Early Development, Oncology R&D, AstraZeneca, Waltham, MA, USA.
Caiyun HouState Key Laboratory of Chemical Biology, Shanghai Institute of Organic Chemistry, Chinese Academy of Sciences, Shanghai, China.
Zhen WangState Key Laboratory of Chemical Biology, Shanghai Institute of Organic Chemistry, Chinese Academy of Sciences, Shanghai, China.
Ke DingState Key Laboratory of Chemical Biology, Shanghai Institute of Organic Chemistry, Chinese Academy of Sciences, Shanghai, China.
Arul M ChinnaiyanMichigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, USA. arul@umich.edu.ORCID http://orcid.org/0000-0001-9282-3415
Irfan A AsanganiDepartment of Cancer Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. asangani@upenn.edu.ORCID http://orcid.org/0000-0001-5381-1702
Funding
XenograftP30CA046592 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI THEODORE S LAWRENCE · 1988 to 2026
$178.2MMICHIGAN MEDICAL SCIENTIST TRAINING PROGRAMT32GM007863 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI COLLINS, KATHLEEN L. · 1985 to 2024
$38.3MTissue/InformaticsP50CA186786 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Robert Timothy Dess · 2014 to 2026
$27.6MExploring Precision Oncology: From Gene Fusions to lncRNAsR35CA231996 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHINNAIYAN, ARUL M · 2018 to 2024
$6.4MMichigan-VUMC Biomarker Characterization CenterU2CCA271854 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ARUL M CHINNAIYAN, Jeffrey John Tosoian · 2022 to 2026
$5.4MRole of MED1 in the AR-dependent transcription in advanced prostate cancerR01CA249210 · NCI · UNIVERSITY OF PENNSYLVANIA · PI ASANGANI, IRFAN AHMED · 2020 to 2024
$1.9MCharacterization of Epigenetic Targets in Prostate CancerR00CA187664 · NCI · UNIVERSITY OF PENNSYLVANIA · PI ASANGANI, IRFAN AHMED · 2015 to 2017
$747kSWI/SNF chromatin remodelers in tumor-associated antigen-specific CD8+ cytotoxic T cellsK00CA245825 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PAROLIA, ABHIJIT · 2021 to 2024
$388kNCI NIH HHS K00 CA245825NCI NIH HHS P30 CA046592NCI NIH HHS P50 CA186786NCI NIH HHS R00 CA187664NCI NIH HHS R01 CA249210NCI NIH HHS R35 CA231996NCI NIH HHS U2C CA271854NIGMS NIH HHS T32 GM007863U.S. Department of Defense (United States Department of Defense) W81XWH-17-0404U.S. Department of Defense (United States Department of Defense) W81XWH-21-1-0500U.S. Department of Health & Human Services | National Institutes of Health (NIH) R00-CA187664U.S. Department of Health & Human Services | National Institutes of Health (NIH) R01-CA249210-0U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI) K00-CA245825U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI) P50-CA186786U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI) R35-CA231996
Abstract
Androgen receptor (AR) is a ligand-responsive transcription factor that drives terminal differentiation of the prostatic luminal epithelia. By contrast, in tumors originating from these cells, AR chromatin occupancy is extensively reprogrammed to activate malignant phenotypes, the molecular mechanisms of which remain unknown. Here, we show that tumor-specific AR enhancers are critically reliant on H3K36 dimethyltransferase activity of NSD2. NSD2 expression is abnormally induced in prostate cancer, where its inactivation impairs AR transactivation potential by disrupting over 65% of its cistrome. NSD2-dependent AR sites distinctively harbor the chimeric FOXA1:AR half-motif, which exclusively comprise tumor-specific AR enhancer circuitries defined from patient specimens. NSD2 inactivation also engenders increased dependency on the NSD1 paralog, and a dual NSD1/2 PROTAC degrader is preferentially cytotoxic in AR-dependent prostate cancer models. Altogether, we characterize NSD2 as an essential AR neo-enhanceosome subunit that enables its oncogenic activity, and position NSD1/2 as viable co-targets in advanced prostate cancer.
Indexed as
Histone-Lysine N-MethyltransferaseProstatic NeoplasmsReceptors, AndrogenAnimalsCarcinogenesisCell Line, TumorGene Expression Regulation, NeoplasticHepatocyte Nuclear Factor 3-alphaHumansMaleMiceRepressor ProteinsAR protein, humanFOXA1 protein, humanHepatocyte Nuclear Factor 3-alphaHistone-Lysine N-MethyltransferaseNSD2 protein, humanReceptors, AndrogenRepressor Proteins
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