2024
CTHRC1+ fibroblasts and SPP1+ macrophages synergistically contribute to pro-tumorigenic tumor microenvironment in pancreatic ductal adenocarcinoma
Li E, Cheung H, Ma S. CTHRC1+ fibroblasts and SPP1+ macrophages synergistically contribute to pro-tumorigenic tumor microenvironment in pancreatic ductal adenocarcinoma. Scientific Reports 2024, 14: 17412. PMID: 39075108, PMCID: PMC11286765, DOI: 10.1038/s41598-024-68109-z.Peer-Reviewed Original ResearchConceptsPancreatic ductal adenocarcinomaTumor-associated macrophagesTumor microenvironmentEpithelial mesenchymal transitionDuctal adenocarcinomaImmune-suppressive tumor microenvironmentPro-tumorigenic tumor microenvironmentPancreatic cancer casesHeterogeneous tumor microenvironmentCombination of single-cellCancer-associated myofibroblastsSurgical resectionMyeloid cellsCurrent therapiesCancer casesLethal cancersSurvival rateExtracellular matrixTreat cancerMesenchymal transitionTherapeutic targetAdenocarcinomaCellular populationsCancerIntercellular interactionsIDHwt glioblastomas can be stratified by their transcriptional response to standard treatment, with implications for targeted therapy
Tanner G, Barrow R, Ajaib S, Al-Jabri M, Ahmed N, Pollock S, Finetti M, Rippaus N, Bruns A, Syed K, Poulter J, Matthews L, Hughes T, Wilson E, Johnson C, Varn F, Brüning-Richardson A, Hogg C, Droop A, Gusnanto A, Care M, Cutillo L, Westhead D, Short S, Jenkinson M, Brodbelt A, Chakrabarty A, Ismail A, Verhaak R, Stead L. IDHwt glioblastomas can be stratified by their transcriptional response to standard treatment, with implications for targeted therapy. Genome Biology 2024, 25: 45. PMID: 38326875, PMCID: PMC10848526, DOI: 10.1186/s13059-024-03172-3.Peer-Reviewed Original ResearchConceptsGBM tumorsTumor microenvironmentNeoplastic cellsResponse to standard treatmentTreatment resistance mechanismsDifferentiated neoplastic cellsSurrounding normal brainResponder subtypesGBM stem cellsAssociated with distinct changesRecurrent tumorsIDHwt glioblastomasTargeted therapyIDH1 mutationStandard treatmentBrain neoplasmsTumorCancer-cellBrain tumorsEffective treatmentNeurotransmitter signalingStem cellsMesenchymal transitionPairs of pre-Subtypes
2023
Mammalian SWI/SNF chromatin remodeling complexes promote tyrosine kinase inhibitor resistance in EGFR-mutant lung cancer
de Miguel F, Gentile C, Feng W, Silva S, Sankar A, Exposito F, Cai W, Melnick M, Robles-Oteiza C, Hinkley M, Tsai J, Hartley A, Wei J, Wurtz A, Li F, Toki M, Rimm D, Homer R, Wilen C, Xiao A, Qi J, Yan Q, Nguyen D, Jänne P, Kadoch C, Politi K. Mammalian SWI/SNF chromatin remodeling complexes promote tyrosine kinase inhibitor resistance in EGFR-mutant lung cancer. Cancer Cell 2023, 41: 1516-1534.e9. PMID: 37541244, PMCID: PMC10957226, DOI: 10.1016/j.ccell.2023.07.005.Peer-Reviewed Original ResearchConceptsMammalian SWI/SNF chromatinSWI/SNF chromatinMSWI/SNF complexesGenome-wide localizationGene regulatory signaturesNon-genetic mechanismsEpithelial cell differentiationEGFR-mutant cellsChromatin accessibilitySNF complexCellular programsRegulatory signaturesTKI-resistant lung cancerGene targetsKinase inhibitor resistanceCell differentiationMesenchymal transitionTKI resistancePharmacologic disruptionTyrosine kinase inhibitor resistanceCell proliferationChromatinInhibitor resistanceEGFR-mutant lungKinase inhibitorsAcetate controls endothelial-to-mesenchymal transition
Zhu X, Wang Y, Soaita I, Lee H, Bae H, Boutagy N, Bostwick A, Zhang R, Bowman C, Xu Y, Trefely S, Chen Y, Qin L, Sessa W, Tellides G, Jang C, Snyder N, Yu L, Arany Z, Simons M. Acetate controls endothelial-to-mesenchymal transition. Cell Metabolism 2023, 35: 1163-1178.e10. PMID: 37327791, PMCID: PMC10529701, DOI: 10.1016/j.cmet.2023.05.010.Peer-Reviewed Original ResearchConceptsTGF-β signalingChronic vascular diseaseTGF-β receptor ALK5Mesenchymal transitionInduction of EndMTVascular diseaseMolecular basisPositive feedback loopReceptor ALK5Cellular levelSMADs 2Novel targetEndMT inductionMetabolic modulationMetabolic basisFibrotic stateSignalingPotential treatmentEndMTTGFDiseaseActivationInductionACSS2PDK4Endothelial-to-mesenchymal transition: advances and controversies
Simons M. Endothelial-to-mesenchymal transition: advances and controversies. Current Opinion In Physiology 2023, 34: 100678. PMID: 37305156, PMCID: PMC10249652, DOI: 10.1016/j.cophys.2023.100678.Peer-Reviewed Original Research
2022
Vascular pathobiology of pulmonary hypertension
Gallardo-Vara E, Ntokou A, Dave J, Jovin D, Saddouk F, Greif D. Vascular pathobiology of pulmonary hypertension. The Journal Of Heart And Lung Transplantation 2022, 42: 544-552. PMID: 36604291, PMCID: PMC10121751, DOI: 10.1016/j.healun.2022.12.012.Peer-Reviewed Original ResearchConceptsPulmonary hypertensionCell typesSmooth muscle cell proliferationEndothelial cell dysfunctionMuscle cell proliferationKruppel-like factor 4Extracellular matrix remodelingHypoxia-inducible factorBox proteinBlood pressurePulmonary arteryInflammatory cellsPulmonary vasculatureMain cell typesVascular pathogenesisVasoactive moleculesCell dysfunctionClinical impactVascular pathobiologyPathological remodelingIntercellular crosstalkLethal diseaseMesenchymal transitionMatrix remodelingGrowth factorEndothelial mechanosensing: A forgotten target to treat vascular remodeling in hypertension?
Tiezzi M, Deng H, Baeyens N. Endothelial mechanosensing: A forgotten target to treat vascular remodeling in hypertension? Biochemical Pharmacology 2022, 206: 115290. PMID: 36241094, DOI: 10.1016/j.bcp.2022.115290.Peer-Reviewed Original ResearchConceptsFuture drug development strategiesMechanistic cuesVascular remodelingNew potential therapeutic approachReceptor complexIon channelsPulmonary arterial hypertensionMechanosensitive organMesenchymal transitionPotential therapeutic approachDrug development strategiesCommon mechanismPleiotropic actionsArterial hypertensionEssential hypertensionEndothelial inflammationTherapeutic approachesBlood flowTissue perfusionVascular integrityHypertensionDistinct diseasesCrucial roleRecent studiesRemodelingBMPR1A promotes ID2–ZEB1 interaction to suppress excessive endothelial to mesenchymal transition
Lee H, Adachi T, Pak B, Park S, Hu X, Choi W, Kowalski PS, Chang CH, Clapham KR, Lee A, Papangeli I, Kim J, Han O, Park J, Anderson DG, Simons M, Jin S, Chun HJ. BMPR1A promotes ID2–ZEB1 interaction to suppress excessive endothelial to mesenchymal transition. Cardiovascular Research 2022, 119: 813-825. PMID: 36166408, PMCID: PMC10409893, DOI: 10.1093/cvr/cvac159.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBone Morphogenetic Protein Receptors, Type IEndothelial CellsEndotheliumEpithelial-Mesenchymal TransitionHypertension, PulmonaryInhibitor of Differentiation Protein 2LungMicePulmonary Arterial HypertensionReceptor, Transforming Growth Factor-beta Type IIZinc Finger E-box-Binding Homeobox 1ConceptsPathogenesis of PAHPulmonary arterial hypertensionEndothelial cellsOnset of PAHAmeliorate pulmonary arterial hypertensionPotential novel therapeutic targetType 1 receptorType 2 receptorEndothelial-mesenchymal transitionNovel therapeutic targetGrowth factor-beta stimulationSmooth muscle cellsBone morphogenetic proteinPAH patientsArterial hypertensionVascular disordersBMP type 1 receptorsResponse of ECsAdult miceEndoMTTherapeutic targetBeta stimulationPathogenesisMesenchymal transitionMuscle cellsIntersections of endocrine pathways and the epithelial mesenchymal transition in endometrial cancer
Gelissen JH, Huang GS. Intersections of endocrine pathways and the epithelial mesenchymal transition in endometrial cancer. Frontiers In Oncology 2022, 12: 914405. PMID: 36052252, PMCID: PMC9424890, DOI: 10.3389/fonc.2022.914405.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsEpithelial-mesenchymal transitionEndometrial cancerMesenchymal transitionRegulation of EMTTherapeutic interventionsInvasive capacityCancer metastasisEpithelial originEndocrine pathwaysMesenchymal phenotypeCancerCancer cellsEndocrine signalingMetastasisSignaling pathwaysCritical regulatorMortalityPathwayPotential avenuesHigh Fluid Shear Stress Inhibits Cytokine‐Driven Smad2/3 Activation in Vascular Endothelial Cells
Deng H, Schwartz MA. High Fluid Shear Stress Inhibits Cytokine‐Driven Smad2/3 Activation in Vascular Endothelial Cells. Journal Of The American Heart Association 2022, 11: e025337. PMID: 35861829, PMCID: PMC9707828, DOI: 10.1161/jaha.121.025337.Peer-Reviewed Original ResearchConceptsInflammatory cytokinesSmad2/3 activationEndothelial cellsNuclear translocationInflammatory cytokine treatmentGrowth factor betaVascular endothelial cellsQuantitative polymerase chain reactionSmad2/3 nuclear translocationTarget gene expressionBackground AtherosclerosisInflammatory mediatorsInflammatory pathwaysPolymerase chain reactionResult of inhibitionCytokine treatmentInhibits CytokineFactor betaMesenchymal transitionHigh fluid shear stressCytokinesEndMTGene expressionLaminar fluid shear stressFluid shear stressGlioma progression is shaped by genetic evolution and microenvironment interactions
Varn F, Johnson K, Martinek J, Huse J, Nasrallah M, Wesseling P, Cooper L, Malta T, Wade T, Sabedot T, Brat D, Gould P, Wöehrer A, Aldape K, Ismail A, Sivajothi S, Barthel F, Kim H, Kocakavuk E, Ahmed N, White K, Datta I, Moon H, Pollock S, Goldfarb C, Lee G, Garofano L, Anderson K, Nehar-Belaid D, Barnholtz-Sloan J, Bakas S, Byrne A, D’Angelo F, Gan H, Khasraw M, Migliozzi S, Ormond D, Paek S, Van Meir E, Walenkamp A, Watts C, Weiss T, Weller M, Palucka K, Stead L, Poisson L, Noushmehr H, Iavarone A, Verhaak R, Consortium T, Varn F, Johnson K, Martinek J, Huse J, Nasrallah M, Wesseling P, Cooper L, Malta T, Wade T, Sabedot T, Brat D, Gould P, Wöehrer A, Aldape K, Ismail A, Sivajothi S, Barthel F, Kim H, Kocakavuk E, Ahmed N, White K, Datta I, Moon H, Pollock S, Goldfarb C, Lee G, Garofano L, Anderson K, Nehar-Belaid D, Barnholtz-Sloan J, Bakas S, Byrne A, D’Angelo F, Gan H, Khasraw M, Migliozzi S, Ormond D, Paek S, Van Meir E, Walenkamp A, Watts C, Weiss T, Weller M, Alfaro K, Amin S, Ashley D, Bock C, Brodbelt A, Bulsara K, Castro A, Connelly J, Costello J, de Groot J, Finocchiaro G, French P, Golebiewska A, Hau A, Hong C, Horbinski C, Kannan K, Kouwenhoven M, Lasorella A, LaViolette P, Ligon K, Lowman A, Mehta S, Miletic H, Molinaro A, Ng H, Niclou S, Niers J, Phillips J, Rabadan R, Rao G, Reifenberger G, Sanai N, Short S, Smitt P, Sloan A, Smits M, Snyder J, Suzuki H, Tabatabai G, Tanner G, Tomaszewski W, Wells M, Westerman B, Wheeler H, Xie J, Yung W, Zadeh G, Zhao J, Palucka K, Stead L, Poisson L, Noushmehr H, Iavarone A, Verhaak R. Glioma progression is shaped by genetic evolution and microenvironment interactions. Cell 2022, 185: 2184-2199.e16. PMID: 35649412, PMCID: PMC9189056, DOI: 10.1016/j.cell.2022.04.038.Peer-Reviewed Original ResearchConceptsSpecific ligand-receptor interactionsMicroenvironment interactionsDNA sequencing dataGlioma progressionLigand-receptor interactionsNeoplastic cellsSignaling programsCell statesSequencing dataGenetic evolutionGenetic changesIDH wild-type tumorsIsocitrate dehydrogenaseMesenchymal transitionSomatic alterationsDistinct mannerActive tumor growthIDH-mutant gliomasPotential targetTherapy resistanceAdult patientsDisease progressionPossible roleCellsTumor growthSubcellular progression of mesenchymal transition identified by two discrete synchronous cell lines derived from the same glioblastoma
Kim S, Park S, Chowdhury T, Hong J, Ahn J, Jeong T, Yu H, Shin Y, Ku J, Park J, Hur J, Lee H, Kim K, Park C. Subcellular progression of mesenchymal transition identified by two discrete synchronous cell lines derived from the same glioblastoma. Cellular And Molecular Life Sciences 2022, 79: 181. PMID: 35278143, PMCID: PMC8918182, DOI: 10.1007/s00018-022-04188-3.Peer-Reviewed Original ResearchConceptsMesenchymal transitionCell linesAvailable single-cell RNA-seq dataMesenchymal transition (EMT) processCancer cell linesSame tissue samplesTherapeutic implicationsTumor samplesRecurrent samplesDriver mutationsGlioblastomaTissue samplesDistinct cancer cell linesGBM samplesIntratumoral heterogeneityTranscriptomic characteristics
2021
Lung Cancer Models Reveal Severe Acute Respiratory Syndrome Coronavirus 2–Induced Epithelial-to-Mesenchymal Transition Contributes to Coronavirus Disease 2019 Pathophysiology
Stewart CA, Gay CM, Ramkumar K, Cargill KR, Cardnell RJ, Nilsson MB, Heeke S, Park EM, Kundu ST, Diao L, Wang Q, Shen L, Xi Y, Zhang B, Della Corte CM, Fan Y, Kundu K, Gao B, Avila K, Pickering CR, Johnson FM, Zhang J, Kadara H, Minna JD, Gibbons DL, Wang J, Heymach JV, Byers LA. Lung Cancer Models Reveal Severe Acute Respiratory Syndrome Coronavirus 2–Induced Epithelial-to-Mesenchymal Transition Contributes to Coronavirus Disease 2019 Pathophysiology. Journal Of Thoracic Oncology 2021, 16: 1821-1839. PMID: 34274504, PMCID: PMC8282443, DOI: 10.1016/j.jtho.2021.07.002.Peer-Reviewed Original ResearchConceptsSevere acute respiratory syndrome coronavirus 2Acute respiratory syndrome coronavirus 2Respiratory syndrome coronavirus 2Syndrome coronavirus 2Coronavirus disease 2019SARS-CoV-2Coronavirus 2Disease 2019Coronavirus disease 2019 pathophysiologyMesenchymal transitionSARS-CoV-2 infectionSARS-CoV-2 pathogenesisSARS-CoV-2 receptorTyrosine kinase inhibitor resistanceEGFR tyrosine kinase inhibitor resistanceRegulation of ZEB1Lung cancer model systemsLung cancer modelKinase inhibitor resistanceCancer cell linesACE2 expressionRegulation of ACE2Respiratory virusesCancer model systemsHealthy patientsLoss of endothelial glucocorticoid receptor accelerates diabetic nephropathy
Srivastava SP, Zhou H, Setia O, Liu B, Kanasaki K, Koya D, Dardik A, Fernandez-Hernando C, Goodwin J. Loss of endothelial glucocorticoid receptor accelerates diabetic nephropathy. Nature Communications 2021, 12: 2368. PMID: 33888696, PMCID: PMC8062600, DOI: 10.1038/s41467-021-22617-y.Peer-Reviewed Original ResearchMeSH KeywordsAdrenalectomyAnimalsDiabetes Mellitus, ExperimentalDiabetic NephropathiesEndothelial CellsEndotheliumEpithelial-Mesenchymal TransitionFatty AcidsFibrosisGlucocorticoidsHumansHypercholesterolemiaInterleukin-6Kidney TubulesMaleMiceMice, Knockout, ApoEOxidation-ReductionReceptors, GlucocorticoidStreptozocinWnt Signaling PathwayConceptsEndothelial glucocorticoid receptorGlucocorticoid receptorEndothelial cell homeostasisDiabetic miceRenal fibrosisEndothelial cellsMesenchymal transitionSevere renal fibrosisTubular epithelial cellsCell homeostasisFatty acid oxidationDiabetic controlDiabetic nephropathyAntifibrotic moleculesIL-6Kidney fibrosisMesenchymal activationRegulation of diseaseOrgan fibrosisAberrant cytokineFibrogenic phenotypeFibrosisMiceEpithelial cellsDefective regulationEndothelial SIRT3 regulates myofibroblast metabolic shifts in diabetic kidneys
Srivastava SP, Li J, Takagaki Y, Kitada M, Goodwin JE, Kanasaki K, Koya D. Endothelial SIRT3 regulates myofibroblast metabolic shifts in diabetic kidneys. IScience 2021, 24: 102390. PMID: 33981977, PMCID: PMC8086030, DOI: 10.1016/j.isci.2021.102390.Peer-Reviewed Original ResearchDiabetic kidney fibrosisDiabetic kidneyEndothelial cellsKidney fibrosisDefective metabolismRenal tubular epithelial cellsTubular epithelial cellsKidney functionDiabetic miceFibrogenic pathwaysFibrogenic processDisease processLoss of functionMesenchymal transitionKidneyMouse strainsEpithelial cellsGain of functionSIRT3Metabolic reprogrammingMesenchymal transformationFibrosisSIRT3 geneMetabolismCells
2020
Anti-Cancer Effects of RAW 264.7 Cells on Prostate Cancer PC-3 Cells.
Nam H, Bae J, Kim Y, An H, Kim S, Kim K, Yu S, Park B, Lee S, Ahn S. Anti-Cancer Effects of RAW 264.7 Cells on Prostate Cancer PC-3 Cells. Annals Of Clinical & Laboratory Science 2020, 50: 739-746. PMID: 33334788.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisCell CommunicationCell Line, TumorCell MovementCoculture TechniquesCulture Media, ConditionedEpithelial-Mesenchymal TransitionHumansImmunotherapy, AdoptiveLipopolysaccharidesMacrophagesMaleMiceNeoplasm InvasivenessPC-3 CellsProstatic NeoplasmsRAW 264.7 CellsTumor MicroenvironmentConceptsPC-3 cellsAnti-cancer effectsProstate cancer PC-3 cellsCancer PC-3 cellsRAW 264.7 cellsTumor cellsHuman prostate cancer PC-3 cellsEMT-specific markersHigher anti-cancer effectEnzyme-linked immunosorbent assayQuantitative polymerase chain reactionAnti-cancer agentsPolymerase chain reactionImmune cellsInhibitor of metastasisTumor parametersTherapeutic targetingTGF-β2Snail-1Mesenchymal transitionTumor microenvironmentMigration markersWestern blotImmunosorbent assayAngiogenic abilityInhibition of MUC1 exerts cell-cycle arrest and telomerase suppression in glioblastoma cells
Kim S, Seo Y, Chowdhury T, Yu H, Lee C, Kim K, Kang H, Kim H, Park S, Kim K, Park C. Inhibition of MUC1 exerts cell-cycle arrest and telomerase suppression in glioblastoma cells. Scientific Reports 2020, 10: 18238. PMID: 33106534, PMCID: PMC7589558, DOI: 10.1038/s41598-020-75457-z.Peer-Reviewed Original ResearchConceptsRole of MUC1Epithelial-mesenchymal transitionMucin 1Cell cycle arrestMUC1 knockdownNormal brain tissueExpression levelsGrowth factor betaTERT expression levelsGBM cell linesOverall survivalTherapeutic targetOncological processHuman gliomasBrain tissueFactor betaMesenchymal transitionPhosphorylation of RB1Diverse cancersGlioblastomaTelomere maintenance mechanismAnticancer mechanismCell proliferationCycle arrestGlioblastoma cellsTranscriptomic responses to hypoxia in endometrial and decidual stromal cells
Rytkönen KT, Heinosalo T, Mahmoudian M, Ma X, Perheentupa A, Elo LL, Poutanen M, Wagner G. Transcriptomic responses to hypoxia in endometrial and decidual stromal cells. Reproduction 2020, 160: 39-51. PMID: 32272449, DOI: 10.1530/rep-19-0615.Peer-Reviewed Original ResearchConceptsDecidual stromal cellsEndometrial stromal fibroblastsEndometriotic stromal cellsStromal cellsInflammatory transcription factorsEpithelial-mesenchymal transitionExpression of JunDCEBP transcription factorsCell typesHealthy endometriumEndometriosis lesionsProgesterone receptorDecidualization processUterine endometriumStromal fibroblastsMesenchymal transitionProgesterone signalingEndometriumHypoxiaHypoxia pathwayTranscription factorsHuman reproductive successDistinct transcriptional statesExpression of genesJun/FosCancer Biology and Prevention in Diabetes
Srivastava SP, Goodwin JE. Cancer Biology and Prevention in Diabetes. Cells 2020, 9: 1380. PMID: 32498358, PMCID: PMC7349292, DOI: 10.3390/cells9061380.Peer-Reviewed Original ResearchConceptsDPP-4 inhibitorsMesenchymal transitionType II diabetes mellitusCancer biologySite-specific cancersDevelopment of hyperglycemiaAnti-diabetic therapyRisk of cancerDipeptidyl peptidase-4New therapeutic approachesPossible mechanistic linkMolecular pathological mechanismsDiabetes mellitusSGLT2 inhibitorsChronic inflammationCancer-causing mechanismsDiabetic conditionsTumor cell extravasationAntidiabetic drugsTherapeutic approachesEpidemiological dataPeptidase-4DiabetesPathological mechanismsGlucocorticoid receptorH19/TET1 axis promotes TGF‐β signaling linked to endothelial‐to‐mesenchymal transition
Cao T, Jiang Y, Li D, Sun X, Zhang Y, Qin L, Tellides G, Taylor HS, Huang Y. H19/TET1 axis promotes TGF‐β signaling linked to endothelial‐to‐mesenchymal transition. The FASEB Journal 2020, 34: 8625-8640. PMID: 32374060, PMCID: PMC7364839, DOI: 10.1096/fj.202000073rrrrr.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCells, CulturedCoronary VesselsEpithelial-Mesenchymal TransitionHuman Umbilical Vein Endothelial CellsHumansMiceMice, Inbred C57BLMice, KnockoutMixed Function OxygenasesProto-Oncogene ProteinsRNA Processing, Post-TranscriptionalRNA, Long NoncodingSignal TransductionTransforming Growth Factor betaConceptsTGF-β signalingCardiovascular diseaseHuman umbilical vein endothelial cellsEndothelial cellsEndothelial activationMesenchymal transitionMouse pulmonary microvascular endothelial cellsPulmonary microvascular endothelial cellsHuman atherosclerotic coronary arteriesAtherosclerotic coronary arteriesMicrovascular endothelial cellsPrimary human umbilical vein endothelial cellsUmbilical vein endothelial cellsAortic endothelial cellsEndothelial dysfunctionVein endothelial cellsCoronary arteryRisk factorsHyperglycemic conditionsH19 expressionAberrant expressionEndMTH19 lncRNATET1 expressionMolecular underpinnings
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