2024
Hyd/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 programs
2020
The actin polymerization factor Diaphanous and the actin severing protein Flightless I collaborate to regulate sarcomere size
Deng S, Silimon R, Balakrishnan M, Bothe I, Juros D, Soffar D, Baylies M. The actin polymerization factor Diaphanous and the actin severing protein Flightless I collaborate to regulate sarcomere size. Developmental Biology 2020, 469: 12-25. PMID: 32980309, PMCID: PMC8279456, DOI: 10.1016/j.ydbio.2020.09.014.Peer-Reviewed Original ResearchConceptsActin thin filamentsFlightless IRegulate thin filament lengthContractile unit of muscleControl actin dynamicsActin polymerization factorsThin filamentsDrosophila flight muscleMyosin thick filamentsThin filament lengthSarcomere sizeActin regulatorsActin dynamicsFlight musclesThick filamentsActinMuscle developmentFilament lengthContractile unitsPolymerization factorsFunction of muscle fibersFilamentsSarcomereRegulationForminLoss of CHD1 Promotes Heterogeneous Mechanisms of Resistance to AR-Targeted Therapy via Chromatin Dysregulation
Zhang Z, Zhou C, Li X, Barnes S, Deng S, Hoover E, Chen C, Lee Y, Zhang Y, Wang C, Metang L, Wu C, Tirado C, Johnson N, Wongvipat J, Navrazhina K, Cao Z, Choi D, Huang C, Linton E, Chen X, Liang Y, Mason C, de Stanchina E, Abida W, Lujambio A, Li S, Lowe S, Mendell J, Malladi V, Sawyers C, Mu P. Loss of CHD1 Promotes Heterogeneous Mechanisms of Resistance to AR-Targeted Therapy via Chromatin Dysregulation. Cancer Cell 2020, 37: 584-598.e11. PMID: 32220301, PMCID: PMC7292228, DOI: 10.1016/j.ccell.2020.03.001.Peer-Reviewed Original ResearchMeSH KeywordsAndrogen AntagonistsAnimalsApoptosisBiomarkers, TumorCell ProliferationChromatinDNA HelicasesDNA-Binding ProteinsDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHigh-Throughput Screening AssaysHumansMaleMiceProstatic Neoplasms, Castration-ResistantReceptors, AndrogenRNA, Small InterferingTranscription FactorsTumor Cells, CulturedXenograft Model Antitumor AssaysConceptsAntiandrogen resistanceChromatin dysregulationCHD1 lossProstate cancerGenomic copy number alterationsRNA-seq analysisResistance to hormonal therapyCopy number alterationsAR-targeted therapiesMetastatic prostate cancerATAC-seqClosed chromatinRNA-seqTranscriptional plasticityTranscription factorsFunctional screeningTranscriptomic changesMechanisms of resistanceHormone therapyLineage programsChromatinCHD1Global changeIntegrated analysisTherapy
2019
The paracrine induction of prostate cancer progression by caveolin-1
Lin C, Yun E, Lo U, Tai Y, Deng S, Hernandez E, Dang A, Chen Y, Saha D, Mu P, Lin H, Li T, Shen T, Lai C, Hsieh J. The paracrine induction of prostate cancer progression by caveolin-1. Cell Death & Disease 2019, 10: 834. PMID: 31685812, PMCID: PMC6828728, DOI: 10.1038/s41419-019-2066-3.Peer-Reviewed Original ResearchConceptsCastration-resistant prostate cancerCancer stem cellsTumor-derived exosomesProstate cancerCav-1Cancer progressionSubpopulation of cancer stem cellsAssociated with stem cell phenotypeCancer immune evasionProstate cancer progressionStem cell capabilitiesStem cell phenotypePromote cancer developmentPresence of Cav-1Heterogeneous cancer cell populationsCancer cell populationsNeuroendocrine differentiationNeuroendocrine transdifferentiationEpithelial-mesenchymal transitionNFkB signaling pathwayTherapeutic resistanceTumor cellsImmune evasionChemotherapeutic resistanceParacrine induction
2017
Acting on identity: Myoblast fusion and the formation of the syncytial muscle fiber
Deng S, Azevedo M, Baylies M. Acting on identity: Myoblast fusion and the formation of the syncytial muscle fiber. Seminars In Cell And Developmental Biology 2017, 72: 45-55. PMID: 29101004, PMCID: PMC5910025, DOI: 10.1016/j.semcdb.2017.10.033.Peer-Reviewed Original Research
2016
Diaphanous regulates SCAR complex localization during Drosophila myoblast fusion
Deng S, Bothe I, Baylies M. Diaphanous regulates SCAR complex localization during Drosophila myoblast fusion. Fly 2016, 10: 178-186. PMID: 27314572, PMCID: PMC5036928, DOI: 10.1080/19336934.2016.1195938.Peer-Reviewed Original ResearchConceptsArp2/3 activationMyoblast fusionFusion siteSCAR activityDrosophila myoblast fusionBranched actin networksRegulate actin dynamicsActin cytoskeletal rearrangementDrosophila to manExtra View articleLoss of SCARCell-cell fusionOrganizing actinActin dynamicsActin rearrangementActin networkCytoskeletal rearrangementsSite of fusionMultinucleated muscle cellsActinComplex localizationDrosophilaWaspsView articleModel system
2015
The Formin Diaphanous Regulates Myoblast Fusion through Actin Polymerization and Arp2/3 Regulation
Deng S, Bothe I, Baylies M. The Formin Diaphanous Regulates Myoblast Fusion through Actin Polymerization and Arp2/3 Regulation. PLOS Genetics 2015, 11: e1005381. PMID: 26295716, PMCID: PMC4546610, DOI: 10.1371/journal.pgen.1005381.Peer-Reviewed Original ResearchConceptsF-actin fociF-actinActin polymerizationCell-cell fusionPodosome formationMyoblast fusionFusion siteElongation of actin filamentsRegulation of actin polymerizationLoss-of-function conditionsActin turnover rateBranched actin regulatorsDrosophila myoblast fusionBranched actin polymerizationPodosome-like structuresF-actin polymerizationF-actin distributionFormation of multinucleated muscle cellsArp2/3 regulatorsBranched actinActin regulatorsActin structuresDynamic filopodiaActin filamentsMutant alleles
2014
Feedback inhibition of ENaC: Acute and chronic mechanisms
Patel A, Yang L, Deng S, Palmer L. Feedback inhibition of ENaC: Acute and chronic mechanisms. Channels 2014, 8: 444-451. PMID: 25483587, PMCID: PMC4594590, DOI: 10.4161/19336950.2014.949190.Peer-Reviewed Original ResearchPI(4,5)P2 regulates myoblast fusion through Arp2/3 regulator localization at the fusion site
Bothe I, Deng S, Baylies M. PI(4,5)P2 regulates myoblast fusion through Arp2/3 regulator localization at the fusion site. Development 2014, 141: 2289-2301. PMID: 24821989, PMCID: PMC4034421, DOI: 10.1242/dev.100743.Peer-Reviewed Original ResearchMeSH KeywordsActin-Related Protein 2-3 ComplexActinsAnimalsCell CommunicationCell MembraneCytoskeletonDrosophila melanogasterGene Expression Regulation, DevelopmentalGenotypeMuscle Fibers, SkeletalMutationMyoblastsPhosphatidylinositol 4,5-DiphosphatePhospholipidsRac GTP-Binding ProteinsSignal TransductionConceptsF-actinRegulation of F-actin dynamicsActivator of actin polymerizationFusion siteF-actin fociMyoblast fusionF-actin dynamicsRegulation of actinCell-cell fusionActin regulatorsActin fociActin remodelingActin polymerizationPhosphoinositide PI(4,5)P2Regulates localizationCytoskeleton signalingOpposing membranesPI(4,5)P2ActinImpaired fusionArp2/3Receptor engagementCytoskeletonRegulationEnrichment
2008
Leaf surface factors of transgenic Bt cotton associated with the feeding behaviors of cotton aphids: A case study on non-target effects
Xue K, Deng S, Wang R, Yan F, Xu C. Leaf surface factors of transgenic Bt cotton associated with the feeding behaviors of cotton aphids: A case study on non-target effects. Science China Life Sciences 2008, 51: 145-156. PMID: 18239893, DOI: 10.1007/s11427-008-0028-6.Peer-Reviewed Original ResearchConceptsNon-Bt cotton lineElectrical penetration graphTransgenic Bt cottonCotton linesBt cottonCotton aphidElectrical penetration graph resultsNon-Bt linesNon-target pestsFeeding behaviorLeaf surface extractsLeaf surface chemicalsCotton plantsNon-target effectsAphis gossypiiLeaf factorsLeaf extractAphidsLeafGlandular trichomesCottonTrichomesFeedingRegression equationChemical analysis