Su Deng
Assistant ProfessorAbout
Research
Publications
2025
Notch as a Driver of Lineage Plasticity and Therapeutic Target in Enzalutamide-Resistant Prostate Cancer.
Jiang Y, Cheng S, Li L, Fraidenburg M, Kim IY, Deng S, Mu P. Notch as a Driver of Lineage Plasticity and Therapeutic Target in Enzalutamide-Resistant Prostate Cancer. BioRxiv 2025 PMID: 40501767, DOI: 10.1101/2025.05.26.656166.Peer-Reviewed Original ResearchPan-cancer Analysis Identified Ectopic RUNX1T1 Associated with Lineage Plasticity.
Jiang Y, Cheng S, Kim IY, Deng S, Mu P. Pan-cancer Analysis Identified Ectopic RUNX1T1 Associated with Lineage Plasticity. BioRxiv 2025 PMID: 40488132, DOI: 10.1101/2025.04.18.649575.Peer-Reviewed Original ResearchAndrogen Deprivation-Induced TET2 Activation Fuels Prostate Cancer Progression via Epigenetic Priming and Slow-Cycling Cancer Cells.
Li L, Cheng S, Xu Y, Deng S, Mu P, Yu X. Androgen Deprivation-Induced TET2 Activation Fuels Prostate Cancer Progression via Epigenetic Priming and Slow-Cycling Cancer Cells. BioRxiv 2025 PMID: 40196510, DOI: 10.1101/2025.03.26.645495.Peer-Reviewed Original Research
2024
Neuroendocrine Differentiation in Prostate Cancer Requires ASCL1.
Rodarte K, Nir Heyman S, Guo L, Flores L, Savage T, Villarreal J, Deng S, Xu L, Shah R, Oliver T, Johnson J. Neuroendocrine Differentiation in Prostate Cancer Requires ASCL1. Cancer Research 2024, 84: 3522-3537. PMID: 39264686, PMCID: PMC11534540, DOI: 10.1158/0008-5472.can-24-1388.Peer-Reviewed Original ResearchConceptsLoss of RB1Prostate cancerAndrogen receptorEmergence of treatment resistanceGenetically engineered mouse modelsLoss of ASCL1Luminal-like tumorsNeuroendocrine prostate cancerDecreased tumor incidencePoor survival outcomesTranscription factor Ascl1In vivo modelsNE differentiationProstatic adenocarcinomaNeuroendocrine differentiationAllograft tumorsProstate organoidsSurvival outcomesLineage plasticityTreatment resistanceNE featuresTumor incidenceNE lineageProgressive cancerAggressive formHyd/UBR5 defines a tumor suppressor pathway that links Polycomb repressive complex to regulated protein degradation in tissue growth control and tumorigenesis
Wen P, Lei H, Deng H, Deng S, Tirado C, Wang M, Mu P, Zheng Y, Pan D. Hyd/UBR5 defines a tumor suppressor pathway that links Polycomb repressive complex to regulated protein degradation in tissue growth control and tumorigenesis. Genes & Development 2024, 38: 675-691. PMID: 39137945, PMCID: PMC11368183, DOI: 10.1101/gad.351856.124.Peer-Reviewed Original ResearchConceptsPolycomb Repressive Complex1Tumor suppressor pathwayTissue growth controlSuppressor pathwayProtein degradationZinc finger genesGrowth controlUbiquitin-mediated degradationE3 ubiquitin ligasePolycomb repressive complexesProtein degradation pathwaysTumor suppressor geneHyperplastic discsFinger genesMammalian homologSubstrate adaptorRepressive complexesUbiquitin ligaseEmbryonic segmentationProtein complexesModel organismsHuman geneticsUpstream regulatorSuppressor geneProstate cancer tumorigenesisZNF397 Deficiency Triggers TET2-driven Lineage Plasticity and AR-Targeted Therapy Resistance in Prostate Cancer
Xu Y, Yang Y, Wang Z, Sjostrom M, Jiang Y, Tang Y, Cheng S, Deng S, Wang C, Gonzalez J, Johnson N, Li X, Li X, Metang L, Mukherji A, Xu Q, Tirado C, Wainwright G, Yu X, Barnes S, Hofstad M, Chen Y, Zhu H, Hanker A, Raj G, Zhu G, He H, Wang Z, Arteaga C, Liang H, Feng F, Wang Y, Wang T, Mu P. ZNF397 Deficiency Triggers TET2-driven Lineage Plasticity and AR-Targeted Therapy Resistance in Prostate Cancer. Cancer Discovery 2024, 14: 1496-1521. PMID: 38591846, PMCID: PMC11285331, DOI: 10.1158/2159-8290.cd-23-0539.Peer-Reviewed Original ResearchConceptsLineage plasticityTherapy resistanceProstate cancerCancer cellsAndrogen receptorResistance to AR-targeted therapiesLuminal lineageAR-targeted therapiesOvercome therapy resistanceTransition of cancer cellsEpigenetic regulatory machineryBona fide coactivatorTherapy responseAR signalingEpigenetic rewiringDrug resistanceTherapeutic strategiesEpigenetic reprogrammingProstateTherapyCancerPhenotypic plasticityRegulatory machineryAndrogenTranscriptional programsAbstract 4311: The interplay of SYNCRIP deficiency, APOBEC activity, and extrachromosomal DNA in castration-resistant prostate cancer drug resistance
Li X, Deng S, Wang C, Wang Y, Mu P. Abstract 4311: The interplay of SYNCRIP deficiency, APOBEC activity, and extrachromosomal DNA in castration-resistant prostate cancer drug resistance. Cancer Research 2024, 84: 4311-4311. DOI: 10.1158/1538-7445.am2024-4311.Peer-Reviewed Original ResearchProstate cancer drug resistanceCancer drug resistanceDrug resistanceProstate cancerTherapy resistanceAmerican Association for Cancer Research annual meetingsResistance to androgen receptor (AR)-targeted therapiesAndrogen receptor (AR)-targeted therapiesIncreased therapy resistanceTumor mutational burdenCRPC cell linesAPOBEC activityCastration-resistant formComplexity of drug resistanceWhole-exome sequencingContribution to drug resistanceDrivers of resistanceIn vivo modelsPatient-derived samplesExtrachromosomal DNAAPOBEC-mediated mutagenesisMutational burdenDNA damageFunctional CRISPR screensTumor behaviorAbstract 5878: ZNF397 loss triggers TET2-driven epigenetic rewiring, lineage plasticity, and AR-targeted therapy resistance
Mu P, Xu Y, Deng S. Abstract 5878: ZNF397 loss triggers TET2-driven epigenetic rewiring, lineage plasticity, and AR-targeted therapy resistance. Cancer Research 2024, 84: 5878-5878. DOI: 10.1158/1538-7445.am2024-5878.Peer-Reviewed Original ResearchLineage plasticityTherapy resistanceAndrogen receptorEpigenetic rewiringCancer cellsAmerican Association for Cancer Research annual meetingsLuminal lineageOvercome therapy resistanceTransition of cancer cellsAbstract Cancer cellsEpigenetic regulatory machineryAR signalingBreast cancerEpigenetic reprogrammingPhenotypic plasticityRegulatory machineryTranscriptional programsTherapyZNF397CancerLineagesClinical interventionsCo-activationCellsRewiring
2023
UBE2J1 is the E2 ubiquitin-conjugating enzyme regulating androgen receptor degradation and antiandrogen resistance
Rodriguez Tirado C, Wang C, Li X, Deng S, Gonzalez J, Johnson N, Xu Y, Metang L, Sundar Rajan M, Yang Y, Yin Y, Hofstad M, Raj G, Zhang S, Lemoff A, He W, Fan J, Wang Y, Wang T, Mu P. UBE2J1 is the E2 ubiquitin-conjugating enzyme regulating androgen receptor degradation and antiandrogen resistance. Oncogene 2023, 43: 265-280. PMID: 38030789, PMCID: PMC10798893, DOI: 10.1038/s41388-023-02890-5.Peer-Reviewed Original ResearchConceptsAberrant androgen receptorProstate cancerAR ubiquitinationAR degradationAntiandrogen therapyResistance to antiandrogen therapyE2 ubiquitin-conjugating enzymeEnhanced AR signalingAndrogen receptor degradersAR protein levelsProstate cancer patientsUbiquitin-conjugating enzymeResistant tumorsPCa tumorsAR signalingAndrogen receptorAntiandrogen treatmentAntiandrogen resistanceAR proteinReceptor degradationProtein levelsOncogenic proteinsTumorTherapyProtein degradation processZNF397 Loss Triggers TET2-driven Epigenetic Rewiring, Lineage Plasticity, and AR-targeted Therapy Resistance in AR-dependent Cancers.
Xu Y, Wang Z, Sjöström M, Deng S, Wang C, Johnson NA, Gonzalez J, Li X, Metang LA, Tirado CR, Mukherji A, Wainwright G, Yu X, Yang Y, Barnes S, Hofstad M, Zhu H, Hanker A, He HH, Chen Y, Wang Z, Raj G, Arteaga C, Feng F, Wang Y, Wang T, Mu P. ZNF397 Loss Triggers TET2-driven Epigenetic Rewiring, Lineage Plasticity, and AR-targeted Therapy Resistance in AR-dependent Cancers. BioRxiv 2023 PMID: 37961351, DOI: 10.1101/2023.10.24.563645.Peer-Reviewed Original Research
Academic Achievements & Community Involvement
News
News
- July 29, 2025
Yale Urology Research [Q2: April-June 2025]
- April 15, 2025
Yale Urology Research [Q1: January-March 2025]
- October 30, 2024
Yale Urology Research [Q3: July-September 2024]
- September 26, 2024
Yale Urology Welcomes Five New Faculty Members