Search results for " WNT"

showing 10 items of 22 documents

Retinoic Acid affects Lung Adenocarcinoma growth by inducing differentiation via GATA6 activation and EGFR and Wnt inhibition

2016

AbstractA fundamental task in cancer research aims at the identification of new pharmacological therapies that can affect tumor growth. Differentiation therapy might exploit this function not only for hematological diseases, such as acute promyelocytic leukemia (APML) but also for epithelial tumors, including lung cancer. Here we show that Retinoic Acid (RA) arrests in vitro and in vivo the growth of Tyrosine Kinase Inhibitors (TKI) resistant Non Small Cell Lung Cancer (NSCLC). In particular, we found that RA induces G0/G1 cell cycle arrest in TKI resistant NSCLC cells and activates terminal differentiation programs by modulating the expression of GATA6, a key transcription factor involved …

0301 basic medicineAcute promyelocytic leukemiaScienceEGFRRetinoic acidMice NudeTretinoinBiologyArticle03 medical and health scienceschemistry.chemical_compoundDifferentiation therapySettore BIO/13 - Biologia ApplicataCarcinoma Non-Small-Cell LungCell Line TumorGATA6 Transcription FactormedicineRetinoic acidAnimalsHumansLung cancerProtein Kinase InhibitorsWnt Signaling PathwayTranscription factorCell ProliferationMultidisciplinaryQRWnt signaling pathwayCell Differentiationmedicine.diseaseG1 Phase Cell Cycle CheckpointsXenograft Model Antitumor Assaysrespiratory tract diseasesErbB Receptorslung cancerAnimals; Carcinoma Non-Small-Cell Lung; Cell Differentiation; Cell Line Tumor; Cell Proliferation; Drug Resistance Neoplasm; ErbB Receptors; G1 Phase Cell Cycle Checkpoints; GATA6 Transcription Factor; Humans; Mice Nude; Protein Kinase Inhibitors; Signal Transduction; Tretinoin; Wnt Signaling Pathway; Xenograft Model Antitumor Assays030104 developmental biologychemistryDrug Resistance NeoplasmImmunologyCancer researchMedicineAdenocarcinomaEngineering sciences. TechnologyTyrosine kinaseSignal Transduction
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Effects of mutations in Wnt/β-catenin, hedgehog, Notch and PI3K pathways on GSK-3 activity—Diverse effects on cell growth, metabolism and cancer

2016

Glycogen synthase kinase-3 (GSK-3) is a serine/threonine kinase that participates in an array of critical cellular processes. GSK-3 was first characterized as an enzyme that phosphorylated and inactivated glycogen synthase. However, subsequent studies have revealed that this moon-lighting protein is involved in numerous signaling pathways that regulate not only metabolism but also have roles in: apoptosis, cell cycle progression, cell renewal, differentiation, embryogenesis, migration, regulation of gene transcription, stem cell biology and survival. In this review, we will discuss the roles that GSK-3 plays in various diseases as well as how this pivotal kinase interacts with multiple sign…

0301 basic medicineMAPK/ERK pathwaySettore MED/06 - Oncologia MedicaCellular differentiationPI3KTargeted therapyGlycogen Synthase Kinase 3Phosphatidylinositol 3-Kinases0302 clinical medicineGSK-3Neoplasmsbeta CateninGSK-3biologyReceptors NotchKinaseWnt signaling pathwayWnt/beta-cateninCell DifferentiationCell biologyGene Expression Regulation Neoplastic030220 oncology & carcinogenesismTORAkt; GSK-3; Hedgehog; Notch; PI3K; Targeted therapy; Therapy resistance; Wnt/beta-catenin; mTORSignal TransductionBeta-cateninNotchAkt GSK-3 Hedgehog mTOR Notch PI3K Targeted therapy Therapy resistance Wnt/beta-cateninCell Survivalmacromolecular substancesNO03 medical and health sciencesAkt; GSK-3 Hedgehog Notch PI3K Targeted therapy Therapy resistance Wnt/beta-catenin mTORAnimalsHumansHedgehog ProteinsProtein kinase BMolecular BiologyPI3K/AKT/mTOR pathwayCell ProliferationAktTherapy resistanceAkt; GSK-3; Hedgehog; mTOR; Notch; PI3K; Targeted therapy; Therapy resistance; Wnt/beta-catenin; Molecular Biology; Cell BiologyCell BiologyWnt ProteinsMicroRNAs030104 developmental biologyMutationCancer researchbiology.proteinTumor Suppressor Protein p53Hedgehog
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Roles of GSK-3 and microRNAs on epithelial mesenchymal transition and cancer stem cells.

2017

// James A. McCubrey 1 , Timothy L. Fitzgerald 2 , Li V. Yang 3 , Kvin Lertpiriyapong 4 , Linda S. Steelman 1 , Stephen L. Abrams 1 , Giuseppe Montalto 5,6 , Melchiorre Cervello 6 , Luca M. Neri 7 , Lucio Cocco 8 , Alberto M. Martelli 8 , Piotr Laidler 9 , Joanna Dulinska-Litewka 9 , Dariusz Rakus 10 , Agnieszka Gizak 10 , Ferdinando Nicoletti 11 , Luca Falzone 11 , Saverio Candido 11 and Massimo Libra 11 1 Department of Microbiology and Immunology, Brody School of Medicine at East Carolina University, Greenville, NC, USA 2 Department of Surgery, Brody School of Medicine at East Carolina University, Greenville, NC, USA 3 Department of Internal Medicine, Hematology/Oncology Section, Brody Sc…

0301 basic medicineOncologyGerontologycancer stem cellsmedicine.medical_specialtyEpithelial-Mesenchymal TransitionReviewPI3KNO03 medical and health sciencesGlycogen Synthase Kinase 30302 clinical medicineCancer stem cellGSK-3Internal medicinemicroRNAmedicineAnimalsHumansPTENEpithelial–mesenchymal transitionProtein kinase BPI3K/AKT/mTOR pathwayGSK-3biologybusiness.industryAnimalCancer stem cellAktWnt signaling pathwayWnt/beta-cateninMicroRNAMicroRNAsGSK-3 cancer stem cells Wnt/beta-catenin PI3K Akt030104 developmental biologyOncology030220 oncology & carcinogenesisNeoplastic Stem Cellsbiology.proteinNeoplastic Stem CellAkt; GSK-3; PI3K; Wnt/beta-catenin; cancer stem cellsbusinessHumanSignal Transduction
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Suppressive role exerted by microRNA-29b-1-5p in triple negative breast cancer through SPIN1 regulation

2017

MiR-29 family dysregulation occurs in various cancers including breast cancers. We investigated miR-29b-1 functional role in human triple negative breast cancer (TNBC) the most aggressive breast cancer subtype. We found that miR-29b-1-5p was downregulated in human TNBC tissues and cell lines. To assess whether miR- 29b-1-5p correlated with TNBC regenerative potential, we evaluated cancer stem cell enrichment in our TNBC cell lines, and found that only MDA-MB-231 and BT-20 produced primary, secondary and tertiary mammospheres, which were progressively enriched in OCT4, NANOG and SOX2 stemness genes. MiR-29b-1-5p expression inversely correlated with mammosphere stemness potential, and miR-29b…

0301 basic medicineOncologycancer stem cellsCarcinogenesisCell Cycle ProteinsTriple Negative Breast NeoplasmsMicroRNA 29b0302 clinical medicineCell MovementSettore BIO/10 - BiochimicaCancer stem cells; MiR-29b-1; SPIN1; Triple-negative breast cancer; Wnt/β-catenin and Akt signaling pathwaysMedicineBreastBreast -- CancerTriple-negative breast cancerWnt signaling pathwayMicroRNANanog Homeobox ProteinGene Expression Regulation NeoplasticOncologyWnt/β-catenin and Akt signaling pathway030220 oncology & carcinogenesisMiR-29b-1Wnt/β-catenin and Akt signaling pathwaysNeoplastic Stem Cellstriple-negative breast cancerFemaleMicrotubule-Associated ProteinsSignal TransductionResearch Papermedicine.medical_specialtycancer stem cellPaclitaxelDown-Regulation03 medical and health sciencesBreast cancerSOX2Cancer stem cellInternal medicineCell Line TumormicroRNAHumansNeoplasm InvasivenessCell ProliferationSPIN1business.industrySOXB1 Transcription Factorsmedicine.diseasePhosphoproteinsMolecular medicineAntineoplastic Agents PhytogenicMicroRNAs030104 developmental biologyDrug Resistance NeoplasmbusinessOctamer Transcription Factor-3
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The EP300/TP53 pathway, a suppressor of the Hippo and canonical WNT pathways, is activated in human hearts with arrhythmogenic cardiomyopathy in the …

2021

Aim Arrhythmogenic cardiomyopathy (ACM) is a primary myocardial disease that typically manifests with cardiac arrhythmias, progressive heart failure and sudden cardiac death (SCD). ACM is mainly caused by mutations in genes encoding desmosome proteins. Desmosomes are cell-cell adhesion structures and hubs for mechanosensing and mechanotransduction. The objective was to identify the dysregulated molecular and biological pathways in human ACM in the absence of overt heart failure. Methods and results Transcriptomes in the right ventricular endomyocardial biopsy samples from three independent individuals carrying truncating mutations in the DSP gene and 5 control samples were analyzed by RNA-S…

0301 basic medicinePhysiologyCardiomyopathy030204 cardiovascular system & hematologyBiologyMechanotransduction CellularBiological pathway03 medical and health sciences0302 clinical medicinePhysiology (medical)medicineHumansMechanotransductionEP300Wnt Signaling PathwayArrhythmogenic Right Ventricular DysplasiaHeart FailureHippo signaling pathwayWnt signaling pathwayArrhythmias CardiacOriginal Articlesmedicine.diseaseCell biologyDeath Sudden Cardiac030104 developmental biologyCardiomyopathy Gene expression Hippo pathway RNA-Sequencing TP53 WNT pathwayHeart failureTumor Suppressor Protein p53Signal transductionCardiomyopathiesCardiology and Cardiovascular MedicineE1A-Associated p300 ProteinCardiovascular Research
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The Hippo Show Must Go On: YAP Activation as a Therapeutic Strategy in Colorectal Cancer

2020

The role of Hippo pathway in colorectal cancer (CRC) initiation and progression has been controversial. In this issue of Cell Stem Cell, Cheung et al. (2020) shed new light on a distinct function of the transcriptional co-activator YAP as a tumor suppressor and Wnt pathway inhibitor in CRC.

0303 health sciencesHippo signaling pathwayColorectal cancerCellWnt signaling pathwayCell BiologyBiologymedicine.diseasedigestive system diseaseslaw.invention03 medical and health sciences0302 clinical medicinemedicine.anatomical_structurelawGeneticsmedicineCancer researchMolecular MedicineSuppressorYAP colorectal cancer Hippo pathway Wnt pathwayStem cellTranscription factor030217 neurology & neurosurgeryFunction (biology)030304 developmental biologyCell Stem Cell
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PORCN mutations in focal dermal hypoplasia: coping with lethality.

2009

Contains fulltext : 81709.pdf (Publisher’s version ) (Closed access) The X-linked dominant trait focal dermal hypoplasia (FDH, Goltz syndrome) is a developmental defect with focal distribution of affected tissues due to a block of Wnt signal transmission from cells carrying a detrimental PORCN mutation on an active X-chromosome. Molecular characterization of 24 unrelated patients from different ethnic backgrounds revealed 23 different mutations of the PORCN gene in Xp11.23. Three were microdeletions eliminating PORCN and encompassing neighboring genes such as EBP, the gene associated with Conradi-Hunermann-Happle syndrome (CDPX2). 12/24 patients carried nonsense mutations resulting in loss …

AdultMaleAdolescentBase SequenceDNA Mutational AnalysisMolecular Sequence DataInfant NewbornInfantMembrane ProteinsGenomic disorders and inherited multi-system disorders [IGMD 3]Focal Dermal HypoplasiaSettore MED/38 - Pediatria Generale E SpecialisticaSettore MED/03 - Genetica MedicaChild PreschoolMutationGoltz syndrome FDH PORCN WNT skewed X-inactivation postzygotic mosaicHumansProtein IsoformsFemaleAmino Acid SequenceChildAcyltransferasesHuman Mutation
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Convergence of Wnt signaling on the HNF4alpha-driven transcription in controlling liver zonation.

2009

Background & Aims: In each hepatocyte, the specific repertoire of gene expression is influenced by its exact location along the portocentrovenular axis of the hepatic lobule and provides a reason for the liver functions compartmentalization defined "metabolic zonation." So far, few molecular players controlling genetic programs of periportal (PP) and perivenular (PV) hepatocytes have been identified; the elucidation of zonation mechanisms remains a challenge for experimental hepatology. Recently, a key role in induction and maintenance of the hepatocyte heterogeneity has been ascribed to Wnt/β-catenin pathway. We sought to clarify how this wide-ranging stimulus integrates with hepatocyte s…

Beta-cateninWnt ProteinCellular differentiationBlotting WesternLiver Stem CellFluorescent Antibody TechniqueMice TransgenicBiologyTransfectionSensitivity and SpecificityAnimals; Blotting Western; Cell Differentiation; Cell Proliferation; Cells Cultured; Fluorescent Antibody Technique; Hepatocyte Nuclear Factor 4; Hepatocytes; Humans; Immunoprecipitation; Mice; Mice Knockout; Mice Transgenic; Reverse Transcriptase Polymerase Chain Reaction; Sensitivity and Specificity; Signal Transduction; Transfection; Wnt Proteins; beta Catenin; GastroenterologyMiceliver zonation; wnt signalling; beta catenin; hnf4Gene expressionmedicineAnimalsHumansImmunoprecipitationHepatocyteCells Culturedbeta CateninCell ProliferationMice KnockoutHepatologyAnimalReverse Transcriptase Polymerase Chain ReactionGastroenterologyWnt signaling pathwayCell DifferentiationMolecular biologyWnt Proteinsmedicine.anatomical_structureHepatocyte nuclear factor 4Hepatocyte Nuclear Factor 4Hepatocytebiology.proteinHepatocytesChromatin immunoprecipitationHumanSignal TransductionGastroenterology
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β-Catenin Activation Regulates Tissue Growth Non–Cell Autonomously in the Hair Stem Cell Niche

2014

Coordinated Hair Growth Wnt/β-catenin signaling is a key pathway that plays a conserved role in regulating stem cell function during adult tissue regeneration. Using time-lapse imaging of live mice, Deschene et al. (p. 1353 ) show that genetic activation of β-catenin within hair follicle stem cells generates axes of hair growth by coordinated cell divisions and cell movements, even when the normal niches—the dermal papillae—are laser-ablated. Activated β-catenin enhances Wnt ligand secretion, and these ligands can then activate Wnt signaling in adjacent cells that do not have activated β-catenin, indicating how activated stem cells could influence neighboring cells during normal growth and …

Beta-cateninWnt ProteinCellular differentiationLigandBiologyLigandsModels BiologicalArticleMiceStem CellmedicineAnimalsStem Cell NicheAnimals; Cell Differentiation; Cell Division; Hair; Hair Follicle; Ligands; Mice; Models Biological; Mutation; Stem Cell Niche; Stem Cells; Tamoxifen; Up-Regulation; Wnt Proteins; beta Catenin; Wnt Signaling Pathway; Medicine (all); MultidisciplinaryWnt Signaling Pathwaybeta CateninMultidisciplinaryintegumentary systemAnimalStem CellsMedicine (all)Regeneration (biology)Mesenchymal stem cellWnt signaling pathwayCell DifferentiationHair follicleUp-RegulationCell biologyWnt ProteinsTamoxifenmedicine.anatomical_structureCateninMutationbiology.proteinStem cellHair FollicleCell DivisionHairScience
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CD44v6 is a marker of constitutive and reprogrammed cancer stem cells driving colon cancer metastasis.

2014

SummaryCancer stem cells drive tumor formation and metastasis, but how they acquire metastatic traits is not well understood. Here, we show that all colorectal cancer stem cells (CR-CSCs) express CD44v6, which is required for their migration and generation of metastatic tumors. CD44v6 expression is low in primary tumors but demarcated clonogenic CR-CSC populations. Cytokines hepatocyte growth factor (HGF), osteopontin (OPN), and stromal-derived factor 1α (SDF-1), secreted from tumor associated cells, increase CD44v6 expression in CR-CSCs by activating the Wnt/β-catenin pathway, which promotes migration and metastasis. CD44v6− progenitor cells do not give rise to metastatic lesions but, when…

CA15-3Animals; Biomarkers Tumor; Bone Morphogenetic Proteins; Carcinogenesis; Colonic Neoplasms; Fibroblasts; Humans; Hyaluronan Receptors; Mice SCID; Neoplasm Metastasis; Neoplasm Proteins; Neoplastic Stem Cells; Phosphatidylinositol 3-Kinases; Prognosis; Protein Kinase Inhibitors; Proto-Oncogene Proteins c-met; Signal Transduction; Treatment Outcome; Wnt Proteins; Cellular Reprogramming; Molecular Medicine; Genetics; Cell BiologyCarcinogenesisWnt ProteinMice SCIDmedicine.disease_causeAnimals; Antigens CD44; Biomarkers Tumor; Bone Morphogenetic Proteins; Carcinogenesis; Colonic Neoplasms; Fibroblasts; Humans; Mice SCID; Neoplasm Metastasis; Neoplasm Proteins; Neoplastic Stem Cells; Phosphatidylinositol 3-Kinases; Prognosis; Protein Kinase Inhibitors; Proto-Oncogene Proteins c-met; Signal Transduction; Treatment Outcome; Wnt Proteins; Cellular ReprogrammingMetastasisMicePhosphatidylinositol 3-KinasesCD44Neoplasm MetastasisCarcinogenesiPhosphoinositide-3 Kinase InhibitorsColonic NeoplasmTumorbiologyProto-Oncogene Proteins c-metCellular ReprogrammingPrognosisAntigens CD44Neoplasm ProteinsNeoplasm MetastasiAnimals; Antigens CD44; Biomarkers Tumor; Bone Morphogenetic Proteins; Carcinogenesis; Colonic Neoplasms; Fibroblasts; Humans; Mice SCID; Neoplasm Metastasis; Neoplasm Proteins; Neoplastic Stem Cells; Phosphatidylinositol 3-Kinases; Prognosis; Protein Kinase Inhibitors; Proto-Oncogene Proteins c-met; Signal Transduction; Treatment Outcome; Wnt Proteins; Cellular Reprogramming; Cell Biology; Molecular Medicine; GeneticsHyaluronan ReceptorsTreatment OutcomeBone Morphogenetic ProteinsColonic NeoplasmsNeoplastic Stem CellsFibroblastMolecular MedicineHepatocyte growth factorStem cellHumanmedicine.drugSignal TransductionPrognosiProtein Kinase InhibitorSCIDNeoplasm ProteinCancer stem cellSettore MED/04 - PATOLOGIA GENERALEmedicineGeneticsBiomarkers TumorAnimalsHumansAntigensProgenitor cellProtein Kinase InhibitorsSettore MED/04 - Patologia GeneraleAnimalBone Morphogenetic Proteincancer metastasisCD44Cell BiologyFibroblastsmedicine.diseaseWnt ProteinsSettore MED/18 - Chirurgia GeneraleImmunologyCancer researchbiology.proteinNeoplastic Stem CellPhosphatidylinositol 3-KinaseCarcinogenesisBiomarkersCell stem cell
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