2021
Deletion of Cdh16 Ksp-cadherin leads to a developmental delay in the ability to maximally concentrate urine in mouse
Thomson R, Dynia DW, Burlein S, Thomson BR, Booth C, Knauf F, Wang T, Aronson P. Deletion of Cdh16 Ksp-cadherin leads to a developmental delay in the ability to maximally concentrate urine in mouse. American Journal Of Physiology. Renal Physiology 2021, 320: f1106-f1122. PMID: 33938239, PMCID: PMC8285649, DOI: 10.1152/ajprenal.00556.2020.Peer-Reviewed Original ResearchConceptsKsp-cadherinCell adhesion moleculeAtypical memberKidney developmentMammalian kidneyAdult mammalian kidneyBasolateral membraneNormal kidney developmentEpithelial cellsAdhesion moleculesMutant animalsExpression analysisSpecific expressionE-cadherin expressionWestern blot analysisEpithelial phenotypePrincipal proteinE-cadherinBlot analysisMouse linesAquaporin-2CadherinCritical roleDevelopmental delayKnockout miceHDAC Inhibition Induces Cell Cycle Arrest and Mesenchymal-Epithelial Transition in a Novel Pleural-Effusion Derived Uterine Carcinosarcoma Cell Line
Stockhammer P, Okumus Ö, Hegedus L, Rittler D, Ploenes T, Herold T, Kalbourtzis S, Bankfalvi A, Sucker A, Kimmig R, Aigner C, Hegedus B. HDAC Inhibition Induces Cell Cycle Arrest and Mesenchymal-Epithelial Transition in a Novel Pleural-Effusion Derived Uterine Carcinosarcoma Cell Line. Pathology & Oncology Research 2021, 27: 636088. PMID: 34257602, PMCID: PMC8262245, DOI: 10.3389/pore.2021.636088.Peer-Reviewed Original ResearchMeSH KeywordsAntineoplastic Combined Chemotherapy ProtocolsBiomarkers, TumorCarcinosarcomaCell Cycle CheckpointsCisplatinEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHistone DeacetylasesHumansMiddle AgedMutationPaclitaxelPhthalazinesPiperazinesPleural Effusion, MalignantPrognosisPyrazolesQuinolinesTumor Cells, CulturedUterine NeoplasmsVorinostatConceptsEpithelial-mesenchymal transitionUterine carcinosarcomaPleural effusionMesenchymal-epithelial transitionCell linesPatient-derived preclinical modelsMalignant pleural effusionMetastatic tumor lesionsVimentin-positive tumorsE-cadherinCarcinosarcoma cell lineInduces cell cycle arrestHistone deacetylase inhibitionFirst-line chemotherapeuticsΒ-catenin expressionE-cadherin expressionPSmad2 expressionCell cycle analysisPositive tumorsAggressive malignancyMetastatic tumorsDisease progressionCell cycle arrestNovel therapiesPreclinical models
2016
Epidermal growth factor receptor targeting alters gene expression and restores the adhesion function of cancerous cells as measured by single cell force spectroscopy
Azadi S, Tafazzoli-Shadpour M, Omidvar R, Moradi L, Habibi-Anbouhi M. Epidermal growth factor receptor targeting alters gene expression and restores the adhesion function of cancerous cells as measured by single cell force spectroscopy. Molecular And Cellular Biochemistry 2016, 423: 129-139. PMID: 27696309, DOI: 10.1007/s11010-016-2831-x.Peer-Reviewed Original ResearchConceptsCell-cell adhesionE-cadherin expressionEpidermal growth factor receptorGrowth factor receptorAdhesion functionCell-cell adhesion forcesCell-cell adhesion functionSingle-cell force spectroscopyFactor receptorAlters gene expressionCell force spectroscopyE-cadherin geneTime PCR analysisBlockade of EGFRTreatment of cellsForce spectroscopy techniquesHuman epithelial cancer cell linesEpithelial cancer cell linesCancerous cellsCell mechanical propertiesEGFR activityGene expressionCell behaviorInhibition of metastasisCancer progressionGli promotes epithelial-mesenchymal transition in human lung adenocarcinomas
Li H, Yue D, Jin JQ, Woodard GA, Tolani B, Luh TM, Giroux-Leprieur E, Mo M, Chen Z, Che J, Zhang Z, Zhou Y, Wang L, Hao X, Jablons D, Wang C, He B. Gli promotes epithelial-mesenchymal transition in human lung adenocarcinomas. Oncotarget 2016, 5: 80415-80425. PMID: 27533453, PMCID: PMC5348330, DOI: 10.18632/oncotarget.11246.Peer-Reviewed Original ResearchMeSH KeywordsA549 CellsAdenocarcinomaAdenocarcinoma of LungAnimalsAntigens, CDAntineoplastic AgentsCadherinsCell MovementEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHedgehog ProteinsHumansLung NeoplasmsMaleMice, NudeMiddle AgedNeoplasm InvasivenessSignal TransductionSmoothened ReceptorTime FactorsTumor BurdenXenograft Model Antitumor AssaysZinc Finger Protein GLI1ConceptsEpithelial-mesenchymal transitionLung adenocarcinomaE-cadherin expressionTumor growthLung adenocarcinoma metastasisPotential therapeutic targetInhibition of GLICell migrationAdenocarcinoma metastasisLung cancerInvasion/metastasisTumor invasion/metastasisIndependent cohortGLI inhibitorsSmall molecule inhibitorsTherapeutic targetAdenocarcinomaHuman lungTherapeutic agentsMetastasisCell invasionWound healingCommon typeRole of GliMolecule inhibitorsALDOA functions as an oncogene in the highly metastatic pancreatic cancer
Ji S, Zhang B, Liu J, Qin Y, Liang C, Shi S, Jin K, Liang D, Xu W, Xu H, Wang W, Wu C, Liu L, Liu C, Xu J, Ni Q, Yu X. ALDOA functions as an oncogene in the highly metastatic pancreatic cancer. Cancer Letters 2016, 374: 127-135. PMID: 26854714, DOI: 10.1016/j.canlet.2016.01.054.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBiomarkers, TumorCadherinsCarcinoma, Pancreatic DuctalCell Line, TumorFructose-Bisphosphate AldolaseGlycolysisHeterograftsHigh-Throughput Screening AssaysHumansMaleMiceMice, NudeNeoplasm InvasivenessNeoplasm MetastasisOncogenesPancreatic NeoplasmsReactive Oxygen SpeciesSignal TransductionConceptsHigh-throughput screening analysisAldolase APancreatic cancerRegulation of c-MycTGF-bE-cadherinAnalyzed gene expression signaturesRegulation of glycolysisResistant to conventional treatmentPancreatic cancer cell line PANC-1Cancer metabolic changesPrognosis of pancreatic cancerTransforming growth factor-bSubgroup of patientsCell line PANC-1Metastasis of pancreatic cancer cellsPoor prognosis of pancreatic cancerExpression regulationGene expression signaturesPancreatic cancer tissue samplesPancreatic cancer cellsGlycolytic genesGrowth factor BE-cadherin expressionCancer tissue samples
2013
Protein kinase a‐dependent pSer675‐β‐catenin, a novel signaling defect in a mouse model of congenital hepatic fibrosis
Spirli C, Locatelli L, Morell CM, Fiorotto R, Morton SD, Cadamuro M, Fabris L, Strazzabosco M. Protein kinase a‐dependent pSer675‐β‐catenin, a novel signaling defect in a mouse model of congenital hepatic fibrosis. Hepatology 2013, 58: 1713-1723. PMID: 23744610, PMCID: PMC3800498, DOI: 10.1002/hep.26554.Peer-Reviewed Original ResearchConceptsAutosomal recessive polycystic kidney diseaseCongenital hepatic fibrosisCaroli's diseaseΒ-cateninHepatic fibrosisRac-1 inhibitionIntrahepatic bile ductsRecessive polycystic kidney diseasePotential therapeutic targetPolycystic kidney diseaseStimulation of cAMPRac-1 activityE-cadherin expressionBile ductKidney diseaseLiver pathologyCystic dysplasiaMouse modelTherapeutic targetTranscriptional activityNuclear translocationDiseasePKA blockerCholangiocytesFibrosis
2012
Glucocorticoids and histone deacetylase inhibitors cooperate to block the invasiveness of basal-like breast cancer cells through novel mechanisms
Law ME, Corsino PE, Jahn SC, Davis BJ, Chen S, Patel B, Pham K, Lu J, Sheppard B, Nørgaard P, Hong J, Higgins P, Kim JS, Luesch H, Law BK. Glucocorticoids and histone deacetylase inhibitors cooperate to block the invasiveness of basal-like breast cancer cells through novel mechanisms. Oncogene 2012, 32: 1316-1329. PMID: 22543582, PMCID: PMC3773700, DOI: 10.1038/onc.2012.138.Peer-Reviewed Original ResearchConceptsE-cadherin localizationE-cadherinPlasma membraneCytoplasmic vesiclesWild-type E-cadherinBreast cancer cellsSerine protease inhibitor plasminogen activator inhibitor-1HDAC inhibitorsCancer cellsBasal-like breast cancer cellsPro-invasive activityGreen fluorescent proteinFull-length formCDCP1 cleavageAnti-invasive functionInhibitor plasminogen activator inhibitor-1MDA-MB-231 cellsHistone deacetylase inhibitorsTriple-negative breast cancerE-cadherin levelsCellular invasionE-cadherin expressionFluorescent proteinCDCP1 proteinOrthotopic xenograft tumors
2011
Loss of E-cadherin expression and outcome among patients with resectable pancreatic adenocarcinomas
Hong SM, Li A, Olino K, Wolfgang CL, Herman JM, Schulick RD, Iacobuzio-Donahue C, Hruban RH, Goggins M. Loss of E-cadherin expression and outcome among patients with resectable pancreatic adenocarcinomas. Modern Pathology 2011, 24: 1237-1247. PMID: 21552209, PMCID: PMC3155013, DOI: 10.1038/modpathol.2011.74.Peer-Reviewed Original ResearchConceptsPancreatic ductal adenocarcinomaE-cadherin expressionPancreatic adenocarcinomaDuctal adenocarcinomaIndependent predictorsPoor outcomeCox proportional hazards regression modelingProportional hazards regression modelingPancreatic cancer outcomesWorse median survivalResectable pancreatic adenocarcinomaMinority of patientsKaplan-Meier analysisE-cadherin statusMedian survivalSurgical resectionWorse prognosisCancer outcomesSubgroup analysisPathological factorsPatient outcomesCell adhesion moleculeMortality riskTissue microarrayPartial loss
2009
Cadherin expression in gastrointestinal tract endometriosis: possible role in deep tissue invasion and development of malignancy
Van Patten K, Parkash V, Jain D. Cadherin expression in gastrointestinal tract endometriosis: possible role in deep tissue invasion and development of malignancy. Modern Pathology 2009, 23: 38-44. PMID: 19898423, DOI: 10.1038/modpathol.2009.127.Peer-Reviewed Original ResearchConceptsDeep tissue invasionGastrointestinal endometriosisDevelopment of malignancyΒ-catenin expressionN-cadherin expressionSecretory endometriumProliferative endometriumTissue invasionN-cadherinE-cadherinPeritoneal endometriotic implantsCases of carcinomaΒ-cateninRepresentative tissue sectionsStrong membranous stainingNormal proliferative endometriumCell surface proteinsE-cadherin expressionColonic endometriosisEndometriotic implantsPeritoneal endometriosisPathology databaseNormal endometriumEndometriotic glandsSurface proteinsMolecular bases for sensitivity to figitumumab (CP-751,871) in NSCLC
Gualberto A, Dolled-Filhart M, Hixon M, Christensen J, Rimm D, Lee A, Wang Y, Pollak M, Paz-Ares L, Karp D. Molecular bases for sensitivity to figitumumab (CP-751,871) in NSCLC. Journal Of Clinical Oncology 2009, 27: 8091-8091. DOI: 10.1200/jco.2009.27.15_suppl.8091.Peer-Reviewed Original ResearchIGF-binding proteinsFree IGF-1IGF-IR overexpressionIGF-IR expressionNSCLC cell linesNSCLC ptsPlasma levelsIGF-1F trialsHigher IGF-IR expressionIGF type 1 receptorBioavailability of IGFIGF-IR pathwaySquamous cell tumorsType 1 receptorIGF-IR inhibitorCell linesLow E-cadherinE-cadherin expressionE-cadherin levelsPhase 2 activitySquamous NSCLCCell histologyClinical benefitSquamous cells
2006
Vitamin D regulates the phenotype of human breast cancer cells
Pendás-Franco N, González-Sancho J, Suárez Y, Aguilera O, Steinmeyer A, Gamallo C, Berciano MT, Lafarga M, Muñoz A. Vitamin D regulates the phenotype of human breast cancer cells. Differentiation 2006, 75: 193-207. PMID: 17288543, DOI: 10.1111/j.1432-0436.2006.00131.x.Peer-Reviewed Original ResearchConceptsSmooth muscle alpha-actinFocal adhesion kinaseBreast cancer cellsHuman breast cancer cellsCancer cellsP-cadherinFocal adhesion plaquesMDA-MB-453Muscle alpha-actinMesenchymal markers N-cadherinMDA-MB-468 cellsAdhesion kinasePlasma membraneAdhesion plaquesMDA-MB-453 cellsLarge cytoplasmic extensionsActin filamentsE-cadherin expressionCell adhesionCell typesN-cadherinAlpha-actinBreast cancer cell linesCancer cell linesLaser confocalE-cadherin Immunohistochemical Expression as a Prognostic Factor in Infiltrating Ductal Carcinoma of the Breast: a Systematic Review and Meta-Analysis
Gould Rothberg BE, Bracken MB. E-cadherin Immunohistochemical Expression as a Prognostic Factor in Infiltrating Ductal Carcinoma of the Breast: a Systematic Review and Meta-Analysis. Breast Cancer Research And Treatment 2006, 100: 139-148. PMID: 16791476, DOI: 10.1007/s10549-006-9248-2.Peer-Reviewed Original ResearchConceptsDuctal breast carcinomaBreast cancer-specific mortalityCancer-specific mortalityE-cadherin expressionCause mortalityBreast carcinomaCohort studyPrognostic markerImmunohistochemical expressionSystematic reviewSubstantial inter-study heterogeneityIndependent negative prognostic indicatorRetrospective cohort studyPrimary study outcomeSummary hazard ratioNegative prognostic indicatorInter-study heterogeneityRandom-effects modelClinical data collectionAbsent E-cadherin expressionNon-significant associationCadherin immunohistochemical expressionHazard ratioPrognostic factorsDuctal carcinoma
2005
Automated Quantitative Analysis of E-Cadherin Expression in Lymph Node Metastases Is Predictive of Survival in Invasive Ductal Breast Cancer
Harigopal M, Berger AJ, Camp RL, Rimm DL, Kluger HM. Automated Quantitative Analysis of E-Cadherin Expression in Lymph Node Metastases Is Predictive of Survival in Invasive Ductal Breast Cancer. Clinical Cancer Research 2005, 11: 4083-4089. PMID: 15930343, DOI: 10.1158/1078-0432.ccr-04-2191.Peer-Reviewed Original ResearchConceptsE-cadherin expressionLymph node metastasisNodal metastasisBreast cancerImproved survivalNode metastasisTissue microarrayNode-positive breast cancerInvasive ductal breast cancerHER2/neu statusAnti-invasive roleInvasive ductal tumorsNode-positive patientsDuctal breast cancerSubset of patientsGood prognostic markerAggressive tumor behaviorStrong E-cadherin expressionHigh E-cadherin expressionCy5-conjugated antibodiesDuctal tumorsMetastatic sitesPrognostic valueTumor sizePrimary tumor
2003
Downregulation of caveolin-1 function by EGF leads to the loss of E-cadherin, increased transcriptional activity of β-catenin, and enhanced tumor cell invasion
Lu Z, Ghosh S, Wang Z, Hunter T. Downregulation of caveolin-1 function by EGF leads to the loss of E-cadherin, increased transcriptional activity of β-catenin, and enhanced tumor cell invasion. Cancer Cell 2003, 4: 499-515. PMID: 14706341, DOI: 10.1016/s1535-6108(03)00304-0.Peer-Reviewed Original ResearchMeSH Keywordsbeta CateninCadherinsCaveolaeCaveolin 1CaveolinsCell AdhesionCell MovementCell NucleusCytoskeletal ProteinsDNA-Binding ProteinsDown-RegulationEndocytosisEpidermal Growth FactorErbB ReceptorsGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansIntercellular JunctionsNeoplasm MetastasisRNA, AntisenseSignal TransductionSnail Family Transcription FactorsTrans-ActivatorsTranscription FactorsTranscriptional ActivationTumor Cells, CulturedConceptsTranscriptional activityCaveolin-1Cell-cell adhesion proteinsCaveolin-1 functionCell-cell adhesionEGF receptor overexpressionE-cadherinCaveolin-dependent endocytosisTCF/LEFTranscriptional repressor SnailComplex cellular changesCaveolin-1 expressionChronic EGF treatmentTumor cell invasionEGF-induced effectsCaveolin-1 downregulationAdhesion proteinsNegative regulationTranscriptional downregulationAntisense RNAGSK-3betaE-cadherin expressionEGF treatmentHuman tumor cellsCell invasion
1997
Vinculin Is Associated with the E-cadherin Adhesion Complex*
Hazan R, Kang L, Roe S, Borgen P, Rimm D. Vinculin Is Associated with the E-cadherin Adhesion Complex*. Journal Of Biological Chemistry 1997, 272: 32448-32453. PMID: 9405455, DOI: 10.1074/jbc.272.51.32448.Peer-Reviewed Original ResearchConceptsE-cadherin complexAdhesion complexesMDA-MB-468 cellsCalcium-dependent cell-cell adhesionE-cadherin adhesion complexAlpha-catenin geneCadherin-dependent adhesionCell-cell adhesionCell adhesion complexesE-cadherinCell linesAlpha-catenin expressionAlpha cateninReciprocal immunoprecipitationCytoplasmic interactionsCoprecipitation analysisAnti-vinculin antibodiesVinculinCadherinCytoplasmic connectionsFusion proteinE-cadherin expressionSame binding siteMDA-MB-468 breast cancer cell lineCell lysatesTranscriptional defects underlie loss of E-cadherin expression in breast cancer.
Ji X, Woodard AS, Rimm DL, Fearon ER. Transcriptional defects underlie loss of E-cadherin expression in breast cancer. Molecular Cancer Research 1997, 8: 773-8. PMID: 9218871.Peer-Reviewed Original ResearchMeSH KeywordsAntimetabolites, AntineoplasticAzacitidineBreast NeoplasmsCadherinsCloning, MolecularDecitabineDNA MethylationDNA-Binding ProteinsGene Expression Regulation, NeoplasticHumansPromoter Regions, GeneticTrans-ActivatorsTranscription Factor AP-2Transcription FactorsTranscription, GeneticTumor Cells, CulturedConceptsE-cad expressionBreast cancerEpithelial cancersHuman breast cancer cell linesMost breast cancersDifferent epithelial cancersBreast cancer cell linesMajority of cancersE-cadherin expressionCancer cell linesCell adhesion moleculeProgression eventsCancerAdhesion moleculesTumor heterogeneityE-cadherinFunctional assaysCell linesSomatic mutationsE-cad geneGene expression differencesExpressionPromoter activityGene expressionReporter gene constructs
1995
Frequent alterations in E-cadherin and alpha- and beta-catenin expression in human breast cancer cell lines.
Pierceall W, Woodard A, Morrow J, Rimm D, Fearon E. Frequent alterations in E-cadherin and alpha- and beta-catenin expression in human breast cancer cell lines. Oncogene 1995, 11: 1319-26. PMID: 7478552.Peer-Reviewed Original ResearchMeSH Keywordsalpha CateninBase Sequencebeta CateninBlotting, SouthernBlotting, WesternBreast NeoplasmsCadherinsCytoskeletal ProteinsFemaleGene DeletionGene ExpressionHumansMolecular Sequence DataMutationOligodeoxyribonucleotidesPolymerase Chain ReactionPolymorphism, Single-Stranded ConformationalReceptor, ErbB-2RibonucleasesTrans-ActivatorsTumor Cells, CulturedConceptsAlpha-catenin proteinE-cadherin transcriptE-cadherinE-cadherin expressionBeta-catenin expressionCell linesBreast cancer cell linesEpithelial cell-cell interactionsCancer cell linesBeta-catenin proteinCancer-derived cell linesMembrane cytoskeletal proteinsCell-cell interactionsBreast cancer-derived cell linesE-cadherin geneHuman breast cancer-derived cell linesLoss of functionTransmembrane proteinAdherens junctionsCytoskeletal matrixCadherin proteinCytoskeletal proteinsTranscript levelsFrequent alterationsSequence alterationsReduced alpha-catenin and E-cadherin expression in breast cancer.
Rimm DL, Sinard JH, Morrow JS. Reduced alpha-catenin and E-cadherin expression in breast cancer. Laboratory Investigation 1995, 72: 506-12. PMID: 7745946.Peer-Reviewed Original ResearchConceptsE-cadherinSteady-state levelsE-cadherin expressionHomotypic cell adhesion proteinMetastatic diseaseCell adhesion proteinsHuman E-cadherinCell-cell interactionsCytoplasmic proteinsTime of biopsyAdhesion proteinsAggressive tumor behaviorAdhesive functionEffector elementsAdhesion cascadeAbsent E-cadherin expressionTypes of cancerJunctional complexesProteinBreast cancerEpithelial tumorsSensitive markerTumor behaviorExpressionCancer
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