Search results for "Snail Family Transcription Factors"

showing 9 items of 9 documents

Chronic myelogenous leukaemia exosomes modulate bone marrow microenvironment through activation of epidermal growth factor receptor

2016

Abstract Chronic myelogenous leukaemia (CML) is a clonal myeloproliferative disorder. Recent evidence indicates that altered crosstalk between CML and mesenchymal stromal cells may affect leukaemia survival; moreover, vesicles released by both tumour and non‐tumour cells into the microenvironment provide a suitable niche for cancer cell growth and survival. We previously demonstrated that leukaemic and stromal cells establish an exosome‐mediated bidirectional crosstalk leading to the production of IL8 in stromal cells, thus sustaining the survival of CML cells. Human cell lines used are LAMA84 (CML cells), HS5 (stromal cells) and bone marrow primary stromal cells; gene expression and protei…

0301 basic medicineStromal cellchronic myeloid leukaemiaEGFRBone Marrow CellsexosomesBiologyInterleukin 8AmphiregulinBone Marrow Stromal Cell03 medical and health sciencesAmphiregulinSettore BIO/13 - Biologia Applicatahemic and lymphatic diseasesCell Line TumorLeukemia Myelogenous Chronic BCR-ABL PositivemedicineCell AdhesionHumansInterleukin 8Epidermal growth factor receptorRNA MessengerPhosphorylationRNA Small InterferingAnnexin A2SNAILMesenchymal stem cellInterleukin-8Cell BiologyOriginal ArticlesMicrovesiclesCell biologyErbB Receptors030104 developmental biologymedicine.anatomical_structureCellular MicroenvironmentMatrix Metalloproteinase 9Cancer cellChronic Myelogenous Leukemia Exosomes; Interleukin 8; Bone Marrow Stromal Cells; EGFRbiology.proteinMolecular MedicineOriginal ArticleBone marrowSnail Family Transcription FactorsChronic Myelogenous Leukemia ExosomeStromal Cellsepidermal growth factor receptor
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GDF11 exhibits tumor suppressive properties in hepatocellular carcinoma cells by restricting clonal expansion and invasion.

2019

Growth differentiation factor 11 (GDF11) has been characterized as a key regulator of differentiation in cells that retain stemness features, despite some controversies in age-related studies. GDF11 has been poorly investigated in cancer, particularly in those with stemness capacity, such as hepatocellular carcinoma (HCC), one of the most aggressive cancers worldwide. Here, we focused on investigating the effects of GDF11 in liver cancer cells. GDF11 treatment significantly reduced proliferation, colony and spheroid formation in HCC cell lines. Consistently, down-regulation of CDK6, cyclin D1, cyclin A, and concomitant upregulation of p27 was observed after 24 h of treatment. Interestingly,…

0301 basic medicine[SDV]Life Sciences [q-bio]Cyclin ACellChick EmbryoChorioallantoic Membrane0302 clinical medicineCell MovementCyclin D1HCCbiologyNeovascularization PathologicCell DifferentiationHep G2 CellsCell cycleCadherinsHuh7 cells3. Good health[SDV] Life Sciences [q-bio]Gene Expression Regulation NeoplasticGrowth Differentiation Factorsmedicine.anatomical_structure030220 oncology & carcinogenesisBone Morphogenetic ProteinsMolecular MedicineLiver cancerCyclin-Dependent Kinase Inhibitor p27Signal Transduction[SDV.CAN]Life Sciences [q-bio]/CancerCyclin ACell cycleHep3B cells03 medical and health sciencesCyclin D1Downregulation and upregulation[SDV.CAN] Life Sciences [q-bio]/CancerAntigens CDCell Line TumorOccludinSpheroids CellularmedicineAnimalsHumansViability assayMolecular BiologyCell Proliferation[SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and GastroenterologyCyclin-Dependent Kinase 6[SDV.MHEP.HEG] Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterology030104 developmental biologyCell cultureGDF11biology.proteinCancer researchCyclin-dependent kinase 6Snail Family Transcription FactorsBiochimica et biophysica acta. Molecular basis of disease
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The transcription factor ZEB1 (deltaEF1) promotes tumour cell dedifferentiation by repressing master regulators of epithelial polarity.

2007

Epithelial to mesenchymal transition (EMT) is implicated in the progression of primary tumours towards metastasis and is likely caused by a pathological activation of transcription factors regulating EMT in embryonic development. To analyse EMT-causing pathways in tumouri-genesis, we identified transcriptional targets of the E-cadherin repressor ZEB1 in invasive human cancer cells. We show that ZEB1 repressed multiple key determinants of epithelial differentiation and cell–cell adhesion, including the cell polarity genes Crumbs3, HUGL2 and Pals1-associated tight junction protein. ZEB1 associated with their endogenous promoters in vivo, and strongly repressed promotor activities in reporter …

AdultCancer ResearchChromatin ImmunoprecipitationCellular differentiationImmunoblottingDown-RegulationBreast NeoplasmsBiologymedicine.disease_causeEpitheliumArticleCell polarityGeneticsmedicineTumor Cells CulturedHumansNeoplasm InvasivenessEpithelial–mesenchymal transitionCell adhesionPromoter Regions GeneticMolecular BiologyTranscription factorEpithelial polarityAgedOligonucleotide Array Sequence AnalysisHomeodomain ProteinsMembrane GlycoproteinsReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingCell PolarityMembrane ProteinsZinc Finger E-box-Binding Homeobox 1Cell DifferentiationMiddle AgedCadherinsCytoskeletal ProteinsMicroscopy FluorescenceCancer cellColonic NeoplasmsCancer researchDisease ProgressionSnail Family Transcription FactorsCarcinogenesisNucleoside-Phosphate KinaseTranscription FactorsOncogene
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The human Lgl polarity gene, Hugl-2, induces MET and suppresses Snail tumorigenesis

2012

Lethal giant larvae proteins have key roles in regulating polarity in a variety of cell types and function as tumour suppressors. A transcriptional programme initiated by aberrant Snail expression transforms epithelial cells to potentially aggressive cancer cells. Although progress in defining the molecular determinants of this programme has been made, we have little knowledge as to how the Snail-induced phenotype can be suppressed. In our studies we identified the human lethal giant larvae homologue 2, Hugl-2, (Llgl2/Lgl2) polarity gene as downregulated by Snail. Snail binds E-boxes in the Hugl-2 promoter and represses Hugl-2 expression, whereas removal of the E-boxes releases Hugl-2 from …

Cancer ResearchCell typeMice SCIDSnailmedicine.disease_causeMiceMice Inbred NODbiology.animalChlorocebus aethiopsparasitic diseasesCell polarityGeneticsmedicineAnimalsHumansGenes Tumor SuppressorNeoplasm MetastasisMolecular BiologyTranscription factorCells CulturedRegulation of gene expressionbiologyfungiHEK 293 cellsCell PolarityHep G2 CellsAnatomyProto-Oncogene Proteins c-metXenograft Model Antitumor AssaysPhenotypeUp-RegulationCell biologyGene Expression Regulation NeoplasticCytoskeletal ProteinsCell Transformation NeoplasticHEK293 CellsCOS CellsSnail Family Transcription FactorsCarcinogenesisProtein BindingTranscription FactorsOncogene
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The inhibitor of differentiation-1 (Id1) enables lung cancer liver colonization through activation of an EMT program in tumor cells and establishment…

2017

Abstract: Id1 promotes carcinogenesis and metastasis, and predicts prognosis of non-small cell lung cancer (NSCLC)-adenocarcionoma patients. We hypothesized that Id1 may play a critical role in lung cancer colonization of the liver by affecting both tumor cells and the microenvironment. Depleted levels of Id1 in LLC (Lewis lung carcinoma cells, LLC shId1) significantly reduced cell proliferation and migration in vitro. Genetic loss of Id1 in the host tissue (Id1(-/-) mice) impaired liver colonization and increased survival of Id1 animals. Histologically, the presence of Idl in tumor cells of liver metastasis was responsible for liver colonization. Microarray analysis comparing liver tumor n…

Inhibitor of Differentiation Protein 10301 basic medicineCancer ResearchPathologyLung NeoplasmsTime Factors10255 Clinic for Thoracic SurgeryVimentinmedicine.disease_causeMetastasisCarcinoma Lewis Lung0302 clinical medicineCell MovementCarcinoma Non-Small-Cell LungTumor Microenvironment1306 Cancer ResearchMice KnockoutTissue microarrayIntegrin beta1Liver NeoplasmsTumor BurdenGene Expression Regulation NeoplasticOncology030220 oncology & carcinogenesis2730 OncologySignal Transductionmedicine.medical_specialtyEpithelial-Mesenchymal TransitionLiver tumor610 Medicine & healthBiologyTransforming Growth Factor beta103 medical and health sciencesCell Line Tumor10049 Institute of Pathology and Molecular PathologymedicineAnimalsHumansVimentinEpithelial–mesenchymal transitionLung cancerCell ProliferationLewis lung carcinomamedicine.diseaseMice Inbred C57BL030104 developmental biologyCancer researchbiology.proteinHuman medicineSnail Family Transcription FactorsCarcinogenesisCancer Letters
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Specific expression patterns of epithelial to mesenchymal transition factors in gestational molar disease.

2015

Introduction The epithelial to mesenchymal transition, a well-known and re-emerging model in pathology, has not been completely investigated in the field of gestational pathology. This study aims at improving the comprehension of this process in molar disease, even looking for new possible immunohistochemical markers. Materials and methods We have analysed the immunohistochemical expression of Twist1 and Snai2, two of the most important transcription factors involved in epithelial to mesenchymal transition, in formalin-fixed paraffin-embedded samples of 23 spontaneous abortive pregnancies, 22 molar pregnancies (10 partial and 12 complete) and 7 term placentas. Results Twist1 and Snai2 were …

MolarPathologymedicine.medical_specialtyStromal cellEpithelial-Mesenchymal TransitionBiologyPregnancymedicineHumansEpithelial–mesenchymal transitionTwistClaudinComplete mole; EMT; Molar disease; Snai2; Twist; Twist1; Obstetrics and Gynecology; Reproductive Medicine; Developmental BiologyCadherinTwist-Related Protein 1EMTObstetrics and GynecologyTrophoblastNuclear ProteinsHydatidiform MoleImmunohistochemistryComplete mole; EMT; Molar disease; Snai2; Twist; Twist1Complete moleSNAI2Molar diseasemedicine.anatomical_structureReproductive MedicineSnai2Case-Control StudiesImmunohistochemistryFemaleSnail Family Transcription FactorsBiomarkersTwist1Developmental BiologyTranscription FactorsPlacenta
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Immunohistochemical study of correlation between histologic subtype and expression of epithelial-mesenchymal transition-related proteins in synovial …

2011

Context.—Synovial sarcomas are mesenchymal tumors with epithelial nature and comprise biphasic and monophasic fibrous subtypes. However, factors determining epithelial or spindle cell differentiation are still unexplored. Aberrant epithelial-mesenchymal transition has been implicated in the pathogenesis of diverse human malignancies.Objective.—To analyze the correlation between cellular phenotype and expression of proteins associated with different epithelial-mesenchymal transition-related pathways.Design.—Immunohistochemical analysis of E-cadherin, Snail, Slug, and dysadherin, components of the Wnt/wingless and PI3K/Akt pathways, was performed on 14 biphasic and 27 monophasic fibrous tumor…

Pathologymedicine.medical_specialtyEpithelial-Mesenchymal TransitionCellBiologyIon ChannelsPathology and Forensic MedicineSarcoma SynovialmedicineBiomarkers TumorHumansEpithelial–mesenchymal transitionMembrane GlycoproteinsMesenchymal stem cellMicrofilament ProteinsGeneral Medicinemedicine.diseaseCadherinsImmunohistochemistryNeoplasm ProteinsMedical Laboratory Technologymedicine.anatomical_structureTissue Array AnalysisSnail Family Transcription FactorsImmunohistochemistrySarcomaSnail Family Transcription FactorsTranscription FactorsArchives of pathologylaboratory medicine
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The stable repression of mesenchymal program is required for hepatocyte identity: A novel role for hepatocyte nuclear factor 4α

2011

The concept that cellular terminal differentiation is stably maintained once development is complete has been questioned by numerous observations showing that differentiated epithelium may undergo an epithelial-to-mesenchymal transition (EMT) program. EMT and the reverse process, mesenchymal-to-epithelial transition (MET), are typical events of development, tissue repair, and tumor progression. In this study, we aimed to clarify the molecular mechanisms underlying these phenotypic conversions in hepatocytes. Hepatocyte nuclear factor 4α (HNF4α) was overexpressed in different hepatocyte cell lines and the resulting gene expression profile was determined by real-time quantitative polymerase…

Transcription FactorCellular differentiationMESH: Mice KnockoutMESH: HepatocytesMesodermMice0302 clinical medicineMESH: Liver NeoplasmsMESH: AnimalsHepatocyteHepatocyte Nuclear Factor 1-alphaMESH: Carcinoma HepatocellularRegulator geneHepatocyte differentiationMice KnockoutMESH: Mesoderm0303 health sciencesLiver NeoplasmsCell DifferentiationMESH: Transcription FactorsCell biologyHepatocyte nuclear factorsPhenotypeMESH: Models AnimalHepatocyte Nuclear Factor 4MESH: Epithelial CellsLiver Neoplasm030220 oncology & carcinogenesisModels AnimalMESH: Hepatocyte Nuclear Factor 4HumanMESH: Cell DifferentiationMESH: Cell Line TumorCarcinoma Hepatocellular[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyMESH: PhenotypeArticle03 medical and health scienceshepatocyte; mesenchymal program; SnailCell Line TumorAnimalsHumansMESH: Hepatocyte Nuclear Factor 1-alphaMESH: MiceTranscription factorAnimals; Carcinoma Hepatocellular; Cell Differentiation; Cell Line Tumor; Epithelial Cells; Hepatocyte Nuclear Factor 1-alpha; Hepatocyte Nuclear Factor 4; Hepatocytes; Humans; Liver Neoplasms; Mesoderm; Mice; Mice Knockout; Models Animal; Phenotype; Snail Family Transcription Factors; Transcription Factors; Hepatology030304 developmental biologyEpithelial CellMESH: HumansHepatologyAnimalMesenchymal stem cellEpithelial CellsSnail Family Transcription FactorMolecular biologyHepatocyte nuclear factor 4HepatocytesSnail Family Transcription FactorsChromatin immunoprecipitationTranscription Factors
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An epistatic mini-circuitry between the transcription factors Snail and HNF4α controls liver stem cell and hepatocyte features exhorting opposite reg…

2011

Preservation of the epithelial state involves the stable repression of epithelial-to-mesenchymal transition program, whereas maintenance of the stem compartment requires the inhibition of differentiation processes. A simple and direct molecular mini-circuitry between master elements of these biological processes might provide the best device to keep balanced such complex phenomena. In this work, we show that in hepatic stem cell Snail, a transcriptional repressor of the hepatocyte differentiation master gene HNF4α, directly represses the expression of the epithelial microRNAs (miRs)-200c and-34a, which in turn target several stem cell genes. Notably, in differentiated hepatocytes HNF4α, p…

Transcription GeneticTranscription FactorCellular differentiationLiver Stem CellSnailMESH: Mice KnockoutMESH: HepatocytesMice0302 clinical medicineSnail; hnf4a; mir-200; mir-34a; stemness; hepatocyte differentiationHepatocyteMESH: AnimalsMice KnockoutHepatocyte differentiationmir-34a0303 health sciencesStemneStem CellsMicroRNACell DifferentiationMESH: Transcription FactorsCell biologySnailmir-200Hepatocyte Nuclear Factor 4Liver030220 oncology & carcinogenesisMiRs-200MESH: Hepatocyte Nuclear Factor 4Hepatocyte differentiation; HNF4a; MiR-34a; MiRs-200; Snail; Stemness; Animals; Cell Differentiation; Epithelial-Mesenchymal Transition; Hepatocyte Nuclear Factor 4; Hepatocytes; Liver; Mice; Mice Knockout; MicroRNAs; Snail Family Transcription Factors; Stem Cells; Transcription Factors; Transcription Genetic; Cell Biology; Molecular BiologyStem cellhnf4aMESH: Cell Differentiationhepatocyte differentiationEpithelial-Mesenchymal TransitionMESH: Stem Cells[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologystemness03 medical and health sciencesStem Cellbiology.animalAnimals[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyEpithelial–mesenchymal transitionMESH: MiceMolecular BiologyTranscription factor030304 developmental biologyOriginal PaperAnimalMESH: Transcription GeneticSnail Family Transcription FactorCell BiologyMolecular biologyMicroRNAsMESH: Epithelial-Mesenchymal TransitionHepatocyte nuclear factor 4HepatocytesSnail Family Transcription FactorsMESH: MicroRNAsMESH: LiverTranscription FactorsCell Death & Differentiation
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