2022
The driver role of JAK‐STAT signalling in cancer stemness capabilities leading to new therapeutic strategies for therapy‐ and castration‐resistant prostate cancer
Lo U, Chen Y, Cen J, Deng S, Luo J, Zhau H, Ho L, Lai C, Mu P, Chung L, Hsieh J. The driver role of JAK‐STAT signalling in cancer stemness capabilities leading to new therapeutic strategies for therapy‐ and castration‐resistant prostate cancer. Clinical And Translational Medicine 2022, 12: e978. PMID: 35908276, PMCID: PMC9339240, DOI: 10.1002/ctm2.978.Peer-Reviewed Original ResearchMeSH KeywordsHumansInterferonsJanus KinasesMaleMicroRNAsProstatic Neoplasms, Castration-ResistantSignal TransductionSTAT Transcription FactorsConceptsCastration-resistant prostate cancerProstate cancerCancer stem cellsActivation of JAKJAK-STAT signalingGene set enrichment analysisJAK-STAT1 pathwaySTAT1 inhibitorAcquisition of stemness propertiesProstate cancer cell linesProstate cancer stemnessAssociated with cancer stem cellsIn vivo anti-tumor activityMetastatic prostate cancerTumor-initiating capabilityJAK-STATProstasphere assayDownstream effectorsIngenuity PathwayGenetic manipulationCSC genesBioinformatics analysisEnrichment analysisJAK-STAT1Signaling pathway
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
2014
PI(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