2022
PRMT4-mediated arginine methylation promotes tyrosine phosphorylation of VEGFR-2 and regulates filopodia protrusions
Hartsough E, Shelke R, Amraei R, Aryan Z, Lotfollahzadeh S, Rahimi N. PRMT4-mediated arginine methylation promotes tyrosine phosphorylation of VEGFR-2 and regulates filopodia protrusions. IScience 2022, 25: 104736. PMID: 35942094, PMCID: PMC9356023, DOI: 10.1016/j.isci.2022.104736.Peer-Reviewed Original ResearchSrc homology domain 2Protein arginine methyltransferase 4N-terminal domain bindsFilopodia protrusionsVEGFR-2Arginine methylationDomain bindsVascular endothelial growth factor receptor 2 activationSignal transductionTyrosine phosphorylationC-SrcMolecular mechanismsDomain 2MethylationPhosphorylationAngiogenic signalingPathological angiogenesisReceptor 2 activationAngiogenic responseTumor angiogenesisVEGFR-2 inhibitorsEVH1AngiogenesisTransductionSignalingALDH1A1 overexpression in melanoma cells promotes tumor angiogenesis by activating the IL-8/Notch signaling cascade
Ciccone V, Terzuoli E, Ristori E, Filippelli A, Ziche M, Morbidelli L, Donnini S. ALDH1A1 overexpression in melanoma cells promotes tumor angiogenesis by activating the IL-8/Notch signaling cascade. International Journal Of Molecular Medicine 2022, 50: 99. PMID: 35656893, PMCID: PMC9186295, DOI: 10.3892/ijmm.2022.5155.Peer-Reviewed Original ResearchConceptsIL-8Endothelial cellsMelanoma cellsTumor cellsALDH1A1 expressionAngiogenic factorsAngiogenic featuresTumor microenvironmentCancer cellsPoor clinical outcomeHigher microvessel densityNumber of cancersPro-angiogenic phenotypeOverexpression of ALDH1A1ALDH1A1 overexpressionClinical outcomesCo-culture systemMicrovessel densityImmunodeficient miceNF-kBProangiogenic factorsMelanoma cancer cellsTumor angiogenesisMelanoma controlStromal cellsSingle-Cell Transcriptomics Revealed Subtype-Specific Tumor Immune Microenvironments in Human Glioblastomas
Xiao Y, Wang Z, Zhao M, Deng Y, Yang M, Su G, Yang K, Qian C, Hu X, Liu Y, Geng L, Xiao Y, Zou Y, Tang X, Liu H, Xiao H, Fan R. Single-Cell Transcriptomics Revealed Subtype-Specific Tumor Immune Microenvironments in Human Glioblastomas. Frontiers In Immunology 2022, 13: 914236. PMID: 35669791, PMCID: PMC9163377, DOI: 10.3389/fimmu.2022.914236.Peer-Reviewed Original ResearchConceptsTumor immune microenvironmentTumor-associated macrophages/microgliaImmune microenvironmentTumor cellsHuman glioblastomaMacrophages/microgliaAggressive brain tumorDifferent tumor subtypesM2-type polarizationNon-malignant cellsPoor prognosisImmune infiltrationPrimary tumorGBM patientsBrain tumorsPatient stratificationTumor subtypesMajor subtypesMalignant cellsTumor angiogenesisCell subtypesTumor microenvironmentPersonalized treatmentGBM cellsIntra-tumor heterogeneityChapter 2 Antiangiogenic drugs: Chemosensitizers for combination cancer therapy
Donnini S, Filippelli A, Ciccone V, Spini A, Ristori E, Ziche M, Morbidelli L. Chapter 2 Antiangiogenic drugs: Chemosensitizers for combination cancer therapy. 2022, 29-66. DOI: 10.1016/b978-0-323-90190-1.00008-1.Peer-Reviewed Original ResearchImmune-competent T cellsAntiangiogenic drugsVascular normalizationT cellsTumor vasculatureTumor microenvironmentTumor areaImmune checkpoint inhibitorsAnticancer drugsCheckpoint inhibitorsImmune therapyAdvanced tumorsCombination therapyPromising chemosensitizerAntiangiogenic therapyTarget therapyTumor disseminationAnticancer chemoClinical developmentEffective deliverySolid tumorsTherapyTumor progressionTumor resistanceTumor angiogenesis
2021
A ligand-insensitive UNC5B splicing isoform regulates angiogenesis by promoting apoptosis
Pradella D, Deflorian G, Pezzotta A, Di Matteo A, Belloni E, Campolungo D, Paradisi A, Bugatti M, Vermi W, Campioni M, Chiapparino A, Scietti L, Forneris F, Giampietro C, Volf N, Rehman M, Zacchigna S, Paronetto MP, Pistocchi A, Eichmann A, Mehlen P, Ghigna C. A ligand-insensitive UNC5B splicing isoform regulates angiogenesis by promoting apoptosis. Nature Communications 2021, 12: 4872. PMID: 34381052, PMCID: PMC8358048, DOI: 10.1038/s41467-021-24998-6.Peer-Reviewed Original ResearchConceptsSplicing isoformsNetrin-1 bindingAlternative splicing factorPost-transcriptional pathwayNetrin-1 receptor UNC5BBlood vessel developmentEndothelial cellsApoptosis-dependent mannerSplicing factorsApoptotic functionTumor angiogenesisNetrin-1Vascular developmentVessel developmentInduces ApoptosisReceptor UNC5BIsoformsApoptosisUNC5BAngiogenesisExonsRegulatorPoor patient outcomesCancer vasculaturePathway
2018
Cucurbitacin B inhibits tumor angiogenesis by triggering the mitochondrial signaling pathway in endothelial cells
Piao X, Gao F, Zhu J, Wang L, Zhao X, Li X, Sheng M, Zhang Y. Cucurbitacin B inhibits tumor angiogenesis by triggering the mitochondrial signaling pathway in endothelial cells. International Journal Of Molecular Medicine 2018, 42: 1018-1025. PMID: 29717773, DOI: 10.3892/ijmm.2018.3647.Peer-Reviewed Original ResearchConceptsTumor angiogenesisChick embryo chorioallantoic membraneHuman umbilical vascular endothelial cellsMitochondrial apoptotic pathwayMitochondrial signaling pathwayCucurbitacin BVascular endothelial growth factor receptorEndothelial growth factor receptorEndothelial cellsApoptotic pathwayActivity of vascular endothelial growth factor receptorsTargeting of tumor angiogenesisGrowth factor receptorAngiogenesis related diseasesSignaling pathwayAssociated with inhibitionEffective targetMolecular mechanismsVascular endothelial cellsEmbryo chorioallantoic membranePotential drug candidatesTumor growthCubsAnti-inflammation effectsFactor receptorUtility of MALDI-TOF mass spectrometry in an outbreak investigation of acute endophthalmitis following intravitreal injection
Angrup A, Krishnamoorthi S, Biswal M, Gautam V, Ray P, Agarwal A, Dogra M, Singh R, Katoch D, Gupta V. Utility of MALDI-TOF mass spectrometry in an outbreak investigation of acute endophthalmitis following intravitreal injection. Journal Of Hospital Infection 2018, 100: e253-e256. PMID: 29605188, DOI: 10.1016/j.jhin.2018.03.032.Peer-Reviewed Original ResearchConceptsIntravitreal injectionMatrix-Assisted Laser Desorption/Ionization Mass SpectrometryLaser desorption/ionization mass spectrometryMass spectrometryIntravitreal injection of bevacizumabDesorption/ionization mass spectrometryTreating choroidal neovascularizationInjection of bevacizumabRecombinant humanized monoclonal antibodyInhibit tumor angiogenesisMALDI-TOF mass spectrometryHuman monoclonal antibodyOff-label useAcute endophthalmitisEndophthalmitis outbreakChoroidal neovascularizationMultiple dosesTumor angiogenesisBevacizumabEarly diagnosisMonoclonal antibodiesStenotrophomonas maltophiliaEndophthalmitisIntravitrealOutbreak investigation
2017
A novel BET family bromodomain inhibitor NHWD‐870 represents a promising therapeutic agent for a broad spectrum of cancers
Yin M, Wang N, Yan Q. A novel BET family bromodomain inhibitor NHWD‐870 represents a promising therapeutic agent for a broad spectrum of cancers. The FASEB Journal 2017, 31 DOI: 10.1096/fasebj.31.1_supplement.979.3.Peer-Reviewed Original ResearchTumor cellsMouse models of small cell lung cancerModels of small cell lung cancerInhibition of tumor angiogenesisSmall cell lung cancerSpectrum of activity in vitroTriple negative breast cancerSingle agent activitySolid tumor indicationsCell lung cancerInhibition of tumor cell growthNegative breast cancerTumor suppression efficacyNHWD-870Xenograft mouse modelTumor cell growthDiverse mechanisms of actionBET family bromodomain inhibitorsMEK1/2 signalingCancer cell linesOvarian cancerMechanism of actionSolid tumorsTumor indicationsTumor angiogenesisTranscriptional Induction of Periostin by a Sulfatase 2–TGFβ1–SMAD Signaling Axis Mediates Tumor Angiogenesis in Hepatocellular Carcinoma
Chen G, Nakamura I, Dhanasekaran R, Iguchi E, Tolosa EJ, Romecin PA, Vera RE, Almada LL, Miamen AG, Chaiteerakij R, Zhou M, Asiedu MK, Moser CD, Han S, Hu C, Banini BA, Oseini AM, Chen Y, Fang Y, Yang D, Shaleh HM, Wang S, Wu D, Song T, Lee JS, Thorgeirsson SS, Chevet E, Shah VH, Fernandez-Zapico ME, Roberts LR. Transcriptional Induction of Periostin by a Sulfatase 2–TGFβ1–SMAD Signaling Axis Mediates Tumor Angiogenesis in Hepatocellular Carcinoma. Cancer Research 2017, 77: 632-645. PMID: 27872089, PMCID: PMC5429157, DOI: 10.1158/0008-5472.can-15-2556.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBiomarkers, TumorBlotting, WesternCarcinoma, HepatocellularCell Adhesion MoleculesChromatin ImmunoprecipitationEnzyme-Linked Immunosorbent AssayGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansImmunohistochemistryKaplan-Meier EstimateLiver NeoplasmsMiceMice, KnockoutNeovascularization, PathologicOligonucleotide Array Sequence AnalysisReal-Time Polymerase Chain ReactionSignal TransductionSmad ProteinsSulfatasesSulfotransferasesTransforming Growth Factor beta1ConceptsHepatocellular carcinomaSulfatase 2Protein periostinMicrovascular densityHCC cellsExtracellular matrix protein periostinTGFβ1/Smad pathwayMetastatic hepatocellular carcinomaLower microvascular densityPoor patient survivalWild-type miceClinical HCC specimensHuman HCC cellsPatient survivalPOSTN levelsAntiangiogenic approachesKO miceRational drug developmentParacrine fashionNumerous tumorsHCC angiogenesisTumor growthEndothelial proliferationTumor angiogenesisHCC specimens
2016
PlGF/VEGFR-1 Signaling Promotes Macrophage Polarization and Accelerated Tumor Progression in Obesity
Incio J, Tam J, Rahbari NN, Suboj P, McManus DT, Chin SM, Vardam TD, Batista A, Babykutty S, Jung K, Khachatryan A, Hato T, Ligibel JA, Krop IE, Puchner SB, Schlett CL, Hoffmman U, Ancukiewicz M, Shibuya M, Carmeliet P, Soares R, Duda DG, Jain RK, Fukumura D. PlGF/VEGFR-1 Signaling Promotes Macrophage Polarization and Accelerated Tumor Progression in Obesity. Clinical Cancer Research 2016, 22: 2993-3004. PMID: 26861455, PMCID: PMC4911258, DOI: 10.1158/1078-0432.ccr-15-1839.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBreast NeoplasmsDiet, High-FatFemaleGlucoseHumansHypoglycemic AgentsMacrophagesMetforminMiceMice, Inbred C57BLMice, KnockoutMice, ObeseNeovascularization, PathologicObesityPancreatic NeoplasmsPlacenta Growth FactorPrognosisSignal TransductionVascular Endothelial Growth Factor Receptor-1ConceptsMouse modelTumor progressionTumor-associated macrophage recruitmentDiet-induced obese mouse modelTumor angiogenesisVEGFR-1Breast cancer mouse modelRole of PlGFBreast cancer patientsTumor immune microenvironmentObese mouse modelPlacental growth factorWild-type C57BL/6Addition of metforminHigh-fat dietTumor immune environmentCancer mouse modelReceptors VEGFR-1Breast cancer modelBreast cancer progressionAntitumor immunityTAM infiltrationImmune environmentInsulin levelsImmune microenvironmentNucleoside reverse transcriptase inhibitors attenuate angiogenesis and lymphangiogenesis by impairing receptor tyrosine kinases signaling in endothelial cells.
Song L, Zhu X, Qiu C, Qin L, Chow S, Yu L. Nucleoside reverse transcriptase inhibitors attenuate angiogenesis and lymphangiogenesis by impairing receptor tyrosine kinases signaling in endothelial cells. The FASEB Journal 2016, 30 DOI: 10.1096/fasebj.30.1_supplement.300.2.Peer-Reviewed Original ResearchAntiretroviral therapyReceptor tyrosine kinasesEndothelial cellsRole of ARTEndothelial mitochondrial dysfunctionHIV-positive patientsMicrovascular endothelial cellsVascular endothelial cellsAortic endothelial cellsNRTI treatmentTyrosine kinaseBlood vessel growthMicrovascular functionImmunodeficiency syndromeInhibitor administrationKaposi's sarcomaClinical challengeNoncommunicable diseasesNRTIsNotch1 pathwayAngiogenic pathwaysLymphangiogenic functionTumor angiogenesisLymphatic endothelial cellsReceptor signaling
2015
VEGF-Induced Expression of miR-17–92 Cluster in Endothelial Cells Is Mediated by ERK/ELK1 Activation and Regulates Angiogenesis
Chamorro-Jorganes A, Lee MY, Araldi E, Landskroner-Eiger S, Fernández-Fuertes M, Sahraei M, del Rey M, van Solingen C, Yu J, Fernández-Hernando C, Sessa WC, Suárez Y. VEGF-Induced Expression of miR-17–92 Cluster in Endothelial Cells Is Mediated by ERK/ELK1 Activation and Regulates Angiogenesis. Circulation Research 2015, 118: 38-47. PMID: 26472816, PMCID: PMC4703066, DOI: 10.1161/circresaha.115.307408.Peer-Reviewed Original ResearchConceptsMiR-17Elk1 activationEndothelial angiogenic functionEC proliferationRegulation of angiogenesisTranscription activationTranscriptional programsGenetic evidenceCluster expressionTumor angiogenesisAngiogenic sproutingVEGF stimulationRescue experimentsRetinal angiogenesisRegulate angiogenesisLines of evidenceEndothelial cell functionAngiogenic switchPhysiological retinal angiogenesisAngiogenic functionDevelopmental retinal angiogenesisCell functionTumor developmentRegulationCrucial mediatorAIP1 Expression in Tumor Niche Suppresses Tumor Progression and Metastasis
Ji W, Li Y, He Y, Yin M, Zhou HJ, Boggon TJ, Zhang H, Min W. AIP1 Expression in Tumor Niche Suppresses Tumor Progression and Metastasis. Cancer Research 2015, 75: 3492-3504. PMID: 26139244, PMCID: PMC4558200, DOI: 10.1158/0008-5472.can-15-0088.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAnimalsBreast NeoplasmsCarrier ProteinsCell Line, TumorEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticGuanylate KinasesHumansMelanoma, ExperimentalMiceNeoplasm MetastasisNeovascularization, PathologicProtein Kinase InhibitorsSignal TransductionTumor MicroenvironmentVascular Endothelial Growth Factor Receptor-2ConceptsEpithelial-mesenchymal transitionPremetastatic niche formationTumor growthAugments tumor growthBreast cancer modelSuppresses tumor progressionVascular endothelial cellsNiche formationSystemic administrationCancer modelVEGFR2 kinase inhibitorTumor neovascularizationTumor progressionTumor angiogenesisTumor microenvironmentTumor cellsEndothelial cellsMetastasisKinase inhibitorsTumor nicheVascular ECsSpecific deletionVascular environmentEMT switchAIP1 geneThe novel tumor angiogenic factor, adrenomedullin-2, predicts survival in pancreatic adenocarcinoma
Hollander LL, Guo X, Salem RR, H. CH. The novel tumor angiogenic factor, adrenomedullin-2, predicts survival in pancreatic adenocarcinoma. Journal Of Surgical Research 2015, 197: 219-224. PMID: 25982376, DOI: 10.1016/j.jss.2014.11.002.Peer-Reviewed Original ResearchConceptsMitogen-activated protein kinase/extracellular signal-regulated kinaseProtein kinase/extracellular signal-regulated kinaseExtracellular signal-regulated kinaseSignal-regulated kinaseTotal cellular levelsAdrenomedullin 2Tumor angiogenesis factorVascular endothelial growth factor 2Microarray technologyGrowth factor 2Cellular levelNovel therapeutic targetPancreatic cancer tissuesProtein expressionFactor 2Angiogenesis factorsTherapeutic targetTumor angiogenic factorsTumor angiogenesisAngiogenic rolePotential roleWorse histologic gradePossible roleCancer tissuesPancreas cancer
2014
ELAVL1 regulates alternative splicing of eIF4E transporter to promote postnatal angiogenesis
Chang SH, Elemento O, Zhang J, Zhuang ZW, Simons M, Hla T. ELAVL1 regulates alternative splicing of eIF4E transporter to promote postnatal angiogenesis. Proceedings Of The National Academy Of Sciences Of The United States Of America 2014, 111: 18309-18314. PMID: 25422430, PMCID: PMC4280608, DOI: 10.1073/pnas.1412172111.Peer-Reviewed Original ResearchConceptsProcessing bodiesAlternative splicingEmbryonic lethal abnormal visionRNA processing bodiesNovel posttranscriptional mechanismRNA regulationMRNA turnoverCellular phenotypesPosttranscriptional mechanismsShort isoformTransporter proteinsCellular behaviorPostnatal angiogenesisAngiogenic mRNAsSplicingSprouting behaviorVascular endothelial cellsPathological angiogenesisFactor 1ELAVL1ProteinReduced revascularizationEndothelial cellsExon 11Tumor angiogenesisCarbamoylating Activity Associated with the Activation of the Antitumor Agent Laromustine Inhibits Angiogenesis by Inducing ASK1-Dependent Endothelial Cell Death
Ji W, Yang M, Praggastis A, Li Y, Zhou HJ, He Y, Ghazvinian R, Cincotta DJ, Rice KP, Min W. Carbamoylating Activity Associated with the Activation of the Antitumor Agent Laromustine Inhibits Angiogenesis by Inducing ASK1-Dependent Endothelial Cell Death. PLOS ONE 2014, 9: e103224. PMID: 25068797, PMCID: PMC4113355, DOI: 10.1371/journal.pone.0103224.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntineoplastic AgentsBiocatalysisCarbamatesCattleCell DeathCells, CulturedEndothelial CellsHumansHydrazinesImmunoblottingIsocyanatesMAP Kinase Kinase Kinase 5Mitogen-Activated Protein Kinase 8Neovascularization, PhysiologicSignal TransductionSulfonamidesThioredoxin Reductase 1ThioredoxinsConceptsTrx reductase 1Non-apoptotic pathwaysEndothelial cellsKinase activityCys residuesASK1Endothelial cell deathReductase 1Cell deathInterstrand DNATrx1Reduced thioredoxinInduces dissociationCell lysatesInhibitor 14Role of methylWhole cellsInhibits angiogenesisInhibition of angiogenesisEC deathFree thiol groupsChloroethylating speciesTumor angiogenesisASK1-JNK/p38CellsGlobal microRNA depletion suppresses tumor angiogenesis
Chen S, Xue Y, Wu X, Le C, Bhutkar A, Bell EL, Zhang F, Langer R, Sharp PA. Global microRNA depletion suppresses tumor angiogenesis. Genes & Development 2014, 28: 1054-1067. PMID: 24788094, PMCID: PMC4035535, DOI: 10.1101/gad.239681.114.Peer-Reviewed Original ResearchConceptsUntranslated regionCRISPR/Multiplexed CRISPR/HIF transcriptional activityHypoxia-inducible factor-1Tumor angiogenesisMicroRNA-binding sitesGenome engineeringExpression profilingTranscriptional activityHypoxia responseBalance of angiogenesisHIF transcriptionMicroRNA deficiencyMicroRNAsFIH1Factor 1Angiogenesis genesDeficient angiogenesisAngiogenesisVEGF productionTranscription
2012
Semaphorins in cancer: Biological mechanisms and therapeutic approaches
Rehman M, Tamagnone L. Semaphorins in cancer: Biological mechanisms and therapeutic approaches. Seminars In Cell And Developmental Biology 2012, 24: 179-189. PMID: 23099250, DOI: 10.1016/j.semcdb.2012.10.005.Peer-Reviewed Original ResearchConceptsResponsive cell typesHallmarks of cancerMultiple experimental approachesEpigenetic changesSemaphorin signalsPhysiological processesCell migrationPivotal signalsCell typesReceptor complexCell proliferationSemaphorinsCancer cellsDifferent semaphorinsBiological mechanismsHuman tumorsTumor progressionMultiple alterationsTumor angiogenesisPathwayExperimental approachFamily membersTumor microenvironmentImportant roleCellsCombined MEK and VEGFR Inhibition in Orthotopic Human Lung Cancer Models Results in Enhanced Inhibition of Tumor Angiogenesis, Growth, and Metastasis
Takahashi O, Komaki R, Smith PD, Jürgensmeier JM, Ryan A, Bekele BN, Wistuba II, Jacoby JJ, Korshunova MV, Biernacka A, Erez B, Hosho K, Herbst RS, O'Reilly MS. Combined MEK and VEGFR Inhibition in Orthotopic Human Lung Cancer Models Results in Enhanced Inhibition of Tumor Angiogenesis, Growth, and Metastasis. Clinical Cancer Research 2012, 18: 1641-1654. PMID: 22275507, PMCID: PMC3306446, DOI: 10.1158/1078-0432.ccr-11-2324.Peer-Reviewed Original ResearchMeSH KeywordsAngiogenesis InhibitorsAnimalsAntineoplastic Combined Chemotherapy ProtocolsBenzimidazolesCarcinoma, Non-Small-Cell LungCell Line, TumorCell ProliferationDisease ProgressionHumansLung NeoplasmsMaleMiceMice, NudeMitogen-Activated Protein KinasesMolecular Targeted TherapyNeovascularization, PathologicPaclitaxelProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)Quinazolinesras ProteinsReceptors, Vascular Endothelial Growth FactorXenograft Model Antitumor AssaysConceptsSignal-regulated kinase kinaseTumor cell proliferationCell proliferationReceptor tyrosine kinasesKinase kinaseAvailable MEK1/2 inhibitorHuman NSCLC cellsTyrosine kinaseVEGF receptor tyrosine kinasesERK phosphorylationNCI-H441MEK1/2 inhibitorApoptotic effectsAdjacent normal tissuesKinaseNSCLC cellsMEK inhibitionAntiangiogenic effectsSignalingOrthotopic human lung cancer modelAvailable potent inhibitorLung tumor growthPotent inhibitorTumor angiogenesisSelumetinib
2010
6.05 In Vitro Vascular Cell Culture Systems – Vascular Smooth Muscle
Martin K, Rzucidlo E, Ding M, Merenick B, Kasza Z, Wagner R, Powell R. 6.05 In Vitro Vascular Cell Culture Systems – Vascular Smooth Muscle. 2010, 69-96. DOI: 10.1016/b978-0-08-046884-6.00705-3.ChaptersVascular smooth muscle cellsPhenotypic modulationInsulin-like growth factor IEndothelial cellsVSMC differentiationPathogenesis of atherosclerosisRapamycin (mTOR) inhibitor rapamycinSerum response factorDedifferentiated vascular smooth muscle cellsGrowth factor INormal vascular physiologyActivated T cellsSmooth muscle cellsContractile protein expressionEffects of drugsT cellsSmooth muscleIntimal hyperplasiaFactor family membersTumor angiogenesisVascular physiologyMature arteriesFactor IMuscle cellsVSMC phenotype
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