Su Deng
Assistant ProfessorAbout
Research
Publications
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 ResearchLoss of SYNCRIP unleashes APOBEC-driven mutagenesis, tumor heterogeneity, and AR-targeted therapy resistance in prostate cancer
Li X, Wang Y, Deng S, Zhu G, Wang C, Johnson N, Zhang Z, Tirado C, Xu Y, Metang L, Gonzalez J, Mukherji A, Ye J, Yang Y, Peng W, Tang Y, Hofstad M, Xie Z, Yoon H, Chen L, Liu X, Chen S, Zhu H, Strand D, Liang H, Raj G, He H, Mendell J, Li B, Wang T, Mu P. Loss of SYNCRIP unleashes APOBEC-driven mutagenesis, tumor heterogeneity, and AR-targeted therapy resistance in prostate cancer. Cancer Cell 2023, 41: 1427-1449.e12. PMID: 37478850, PMCID: PMC10530398, DOI: 10.1016/j.ccell.2023.06.010.Peer-Reviewed Original ResearchConceptsProstate cancerTherapy resistanceTumor heterogeneityTumor mutational burdenCell-intrinsic mechanismsPromote tumor heterogeneityMutational burdenTargeted therapyDriver mutationsPCa cellsCancer cellsHuman cancersMutated genesCancerMutational signaturesProstateTumorTherapyFOXA1APOBEC proteinsAPOBEC3BEP300Molecular brakeMutationsSYNCRIPAbstract PR004: Exploring the role of ASCL1 in neuroendocrine prostate cancer
Rodarte K, Flores L, Kandagatla V, Villarreal J, Savage T, Deng S, Mu P, Shah R, Oliver T, Johnson J. Abstract PR004: Exploring the role of ASCL1 in neuroendocrine prostate cancer. Cancer Research 2023, 83: pr004-pr004. DOI: 10.1158/1538-7445.prca2023-pr004.Peer-Reviewed Original ResearchSmall cell lung carcinomaGenetically engineered mouse modelsNeuroendocrine prostate cancerSmall cell histologyCell histologyLoss of RB1Prostatic adenocarcinomaProstate cancerNeuroendocrine markersAndrogen receptorMost patientsNeuroendocrine prostate cancer tumorsNeuroendocrine lineageAdenovirus expressing Cre recombinaseLoss of ASCL1Tumor cell growth in vitroProstate tumor formationCell lung carcinomaExpressing Cre recombinaseLineage programsCell growth in vitroPoor survival outcomesProstate cancer researchSmall cell featuresTranscription factor Ascl1Abstract 3891: Epigenetic rewiring promotes antiandrogen resistance and metastasis via heterogenous oncogenic drivers in prostate cancer
li X, Deng S, Gonzalez J, Tirado C, Wang C, Johnson N, Metang L, Mu P. Abstract 3891: Epigenetic rewiring promotes antiandrogen resistance and metastasis via heterogenous oncogenic drivers in prostate cancer. Cancer Research 2023, 83: 3891-3891. DOI: 10.1158/1538-7445.am2023-3891.Peer-Reviewed Original ResearchResistant prostate cancerProstate cancerAntiandrogen resistanceAndrogen receptorResistant subclonesAmerican Association for Cancer Research annual meetingsOncogenic driversAggressive stage of prostate cancerCastration resistant prostate cancerStaging of prostate cancerGenomic copy number alterationsOvercome resistanceResistant tumor clonesMonths to 2 yearsTargeted therapy drugsResistance to antiandrogensAbstract Prostate cancerCopy number alterationsIncreased tumor heterogeneityDevelopment of novel biomarkersTherapy many patientsAntiandrogenic responseGeneration antiandrogensLoss of Chd1RB1 alterations