Yaru Xu
Associate Research ScientistAbout
Research
Publications
2025
Androgen 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
ZNF397 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 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 processLoss 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 brakeMutationsSYNCRIP
2022
Author Correction: Ectopic JAK–STAT activation enables the transition to a stem-like and multilineage state conferring AR-targeted therapy resistance
Deng S, Wang C, Wang Y, Xu Y, Li X, Johnson N, Mukherji A, Lo U, Xu L, Gonzalez J, Metang L, Ye J, Tirado C, Rodarte K, Zhou Y, Xie Z, Arana C, Annamalai V, Liu X, Vander Griend D, Strand D, Hsieh J, Li B, Raj G, Wang T, Mu P. Author Correction: Ectopic JAK–STAT activation enables the transition to a stem-like and multilineage state conferring AR-targeted therapy resistance. Nature Cancer 2022, 3: 1271-1271. PMID: 36241729, PMCID: PMC9586863, DOI: 10.1038/s43018-022-00458-y.Peer-Reviewed Original ResearchEctopic JAK–STAT activation enables the transition to a stem-like and multilineage state conferring AR-targeted therapy resistance
Deng S, Wang C, Wang Y, Xu Y, Li X, Johnson N, Mukherji A, Lo U, Xu L, Gonzalez J, Metang L, Ye J, Tirado C, Rodarte K, Zhou Y, Xie Z, Arana C, Annamalai V, Liu X, Vander Griend D, Strand D, Hsieh J, Li B, Raj G, Wang T, Mu P. Ectopic JAK–STAT activation enables the transition to a stem-like and multilineage state conferring AR-targeted therapy resistance. Nature Cancer 2022, 3: 1071-1087. PMID: 36065066, PMCID: PMC9499870, DOI: 10.1038/s43018-022-00431-9.Peer-Reviewed Original ResearchConceptsJAK-STAT activationJanus kinase (JAK)-signal transducerTherapy resistanceLineage plasticityTranscriptional programsJAK-STATAR-targeted therapiesLineage programsLineagesMolecular mechanismsTranscriptomic aberrationsPharmaceutical inhibitionProstate cancerTargeted therapyStem-likeTherapeutic targetTherapy
2018
The characterization and potential roles of bone morphogenetic protein 7 during spermatogenesis in Chinese mitten crab Eriocheir sinensis
Xu Y, Wang G, Zhou Y, Yang W. The characterization and potential roles of bone morphogenetic protein 7 during spermatogenesis in Chinese mitten crab Eriocheir sinensis. Gene 2018, 673: 119-129. PMID: 29890312, DOI: 10.1016/j.gene.2018.06.020.Peer-Reviewed Original ResearchConceptsChinese mitten crab Eriocheir sinensisMature spermCrab Eriocheir sinensisBone morphogenetic proteinSelf-renewal of spermatogoniaTranslational levelEriocheir sinensisGonadal developmentCytoplasm of spermatocytesMale gonadal developmentAmino acid sequenceIn situ hybridizationCytoplasm of spermatogoniaReproductive systemSequence conservationQuantitative real-time PCRPhylogenetic analysisTestis developmentAcid sequenceBioinformatics analysisReal-time PCRBMP7 proteinSpermatogoniaProtein signalingWestern blot resultsRoles of three Es-Caspases during spermatogenesis and Cadmium-induced apoptosis in Eriocheir sinensis
Xu Y, Yang W. Roles of three Es-Caspases during spermatogenesis and Cadmium-induced apoptosis in Eriocheir sinensis. Aging 2018, 10: 1146-1165. PMID: 29851651, PMCID: PMC5990378, DOI: 10.18632/aging.101454.Peer-Reviewed Original ResearchConceptsCadmium-induced apoptosisEarly-stage spermatidsFunctions of caspasesAcrosome tubeAcrosomal vesicleMature spermSperm cellsApoptosis-related factorsSinensis,Apoptotic inductionIntrinsic pathwaySpermatogenesisCaspaseExpression patternsApoptosisEriocheir sinensisP53Molecular interactionsPathwayPositive alterationsSpermiogenesisSpermatidsCellsSpermImmunostaining intensityThe role of FSH and TGF-β superfamily in follicle atresia
Chu Y, Xu Y, Yang W, Sun Y. The role of FSH and TGF-β superfamily in follicle atresia. Aging 2018, 10: 305-321. PMID: 29500332, PMCID: PMC5892684, DOI: 10.18632/aging.101391.Peer-Reviewed Original ResearchConceptsInsulin receptor substrateProtein kinase ANon-Smad signalingReceptor substrateApoptosis of granulosa cellsFollicle atresiaRegulatory functionsMolecular mechanismsKinase API3K/Akt pathwayFollicle stimulating hormoneApoptosisTGF-bFactor BFamily membersMammalian folliclesGrowth factor BSuperfamilyGranulosa cells