Search results for "Suppressor"

showing 10 items of 532 documents

The human protein Hugl-1 substitutes for Drosophila lethal giant larvae tumour suppressor function in vivo

2004

Drosophila lethal giant larvae: (lgl), discs large (dlg) and scribble (scrib) are tumour suppressor genes acting in a common pathway, whose loss of function leads to disruption of cell polarity and tissue architecture, uncontrolled proliferation and growth of neoplastic lesions. Mammalian homologues of these genes are highly conserved and evidence is emerging concerning their role in cell proliferation control and tumorigenesis in humans. Here we investigate the functional conservation between Drosophila lethal giant larvae and its human homologue Hugl-1(Llgl1). We first show that Hugl-1 is lost in human solid malignancies, supporting its role as a tumour suppressor in humans. Hugl-1 expres…

SCRIBCancer ResearchTumor suppressor geneBiologymedicine.disease_causeEyelaw.inventionlawDrosophilidaeCell polarityGeneticsmedicineAnimalsDrosophila ProteinsHumansRNA MessengerMolecular BiologyGeneticsCell growthTumor Suppressor ProteinsfungiCell polarity; Drosophila; Epithelial cancers; Hugl-1; Lethal giant larvae; Tumour suppressorGene Expression Regulation DevelopmentalMembrane ProteinsProteinsHugl-1Lethal giant larvaebiology.organism_classificationCell biologyCytoskeletal ProteinsLarvaCell polaritySuppressorDrosophilaDrosophila melanogasterEpithelial cancersCarcinogenesisTumour suppressorProtein Binding
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Suppressor of cytokine signaling 3 sensitizes anaplastic thyroid cancer to standard chemotherapy

2009

We previously showed that cancer cells from papillary, follicular, and anaplastic thyroid carcinomas produce interleukin-4 and interleukin-10, which counteract the cytotoxic activity of conventional chemotherapy through the up-regulation of antiapoptotic molecules. Here, we identify Janus kinase/signal transducers and activators of transcription (STAT) and phosphatidyl inositol 3-kinase (PI3K)/AKT as the down-stream pathways through which these cytokines confer resistance to cell death in thyroid cancer. We found that the absence of suppressors of cytokine signaling (SOCS) molecules allows the propagation of the survival signaling. Exogenous expression of SOCS1, SOCS3, and SOCS5 in the high…

STAT3 Transcription FactorCancer ResearchCancer Research; OncologyDown-RegulationMice NudeSuppressor of Cytokine Signaling Proteinsthyroidcancer spheres cytokines apoptosis chemoterapyMicePhosphatidylinositol 3-KinasesSuppressor of Cytokine Signaling 1 ProteinMedicineAnimalsHumansSOCS3Thyroid NeoplasmsAnaplastic thyroid cancerPhosphorylationThyroid cancerPI3K/AKT/mTOR pathwayAgedSettore MED/04 - Patologia GeneraleJanus kinase 1business.industrySuppressor of cytokine signaling 1Settore BIO/16 - Anatomia UmanaGene Transfer TechniquesCancerJanus Kinase 1Middle Agedmedicine.diseaseXenograft Model Antitumor AssaysSettore MED/18 - Chirurgia GeneraleOncologyDrug Resistance NeoplasmSuppressor of Cytokine Signaling 3 ProteinImmunologyCancer researchFemalebusinessJanus kinaseSTAT6 Transcription FactorProto-Oncogene Proteins c-akt
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Parthenolide sensitizes hepatocellular carcinoma cells to trail by inducing the expression of death receptors through inhibition of STAT3 activation

2011

This article shows that HepG2, Hep3B, and SK-Hep1 cells, three lines of human hepatocellular carcinoma (HCC) cells, are resistant to apoptosis induced by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). Parthenolide, a sesquiterpene lactone found in European feverfew, has been shown to exert both anti-inflammatory and anti-cancer activities. This article demonstrates that co-treatment with parthenolide and TRAIL-induced apoptosis with synergistic interactions in the three lines of HCC cells. In order to explain these effects we ascertained that parthenolide increased either at protein or mRNA level the total content of death receptors TRAIL-R1 and -R2 as well as their surfac…

STAT3 Transcription FactorCarcinoma HepatocellularPhysiologyClinical BiochemistryCellDown-RegulationTRAILApoptosisPharmacologyParthenolideSTAT3TNF-Related Apoptosis-Inducing Ligandchemistry.chemical_compoundSettore BIO/10 - BiochimicamedicineHumansParthenolidePhosphorylationReceptorSTAT3CaspaseJanus KinasesbiologyLiver NeoplasmsProto-Oncogene Proteins c-mdm2Hep G2 CellsReceptors Death DomainCell BiologyapoptosiEnzyme ActivationGene Expression Regulation Neoplasticmedicine.anatomical_structurechemistryCell cultureApoptosisCaspasesbiology.proteinSTAT proteinDrug Screening Assays AntitumorTumor Suppressor Protein p53SesquiterpenesJournal of Cellular Physiology
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Signaling molecules: the pathogenic role of the IL-6/STAT-3 trans signaling pathway in intestinal inflammation and in colonic cancer.

2008

Although the precise etiology of inflammatory bowel diseases (IBD) still remains unclear, considerable progress has been made in the identification of novel signal transduction pathways that elucidate the immunopathogenesis involved in the perpetuation of the inflammatory process. As both ulcerative colitis and Crohn's disease are associated with an increased risk for developing colorectal cancer (CRC) and precancerous dysplastic epithelial changes, further studies have concentrated on finding a common signaling pathway that could serve as a mechanistic link between inflammation and associated colonic cancer in IBD. This review presents the current data concerning the pathogenic role of the…

STAT3 Transcription FactorCell signalingColorectal cancerClinical BiochemistryAnti-Inflammatory AgentsInflammationAntineoplastic AgentsDiseaseSuppressor of cytokine signallingDrug DiscoverymedicineAnimalsHumansAutocrine signallingPharmacologybusiness.industryInterleukin-6medicine.diseaseInflammatory Bowel DiseasesUlcerative colitisdigestive system diseasesCell Transformation NeoplasticColonic NeoplasmsCancer researchMolecular Medicinemedicine.symptomSignal transductionbusinessSignal TransductionCurrent drug targets
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Socs3 induction by PPARγ restrains cancer-promoting inflammation

2013

The presence of proinflammatory cytokines in the tumor microenvironment can support further growth of established cancers. Docosahexaenoic acid (DHA), a peroxisome proliferator-activated receptor-gamma (PPARγ) ligand, has been shown to suppress inflammation and limit tumor progression in vivo. Are the anticancer properties of DHA relying on its ability to prevent inflammation? If so, what are the molecular links between the anti-inflammatory properties of DHA and its anticancer effects? DHA is an n-3 polyinsaturated fatty acid mainly found in fish oil that was shown to contribute to inflammation resolution by preventing the release of proinflammatory mediators in vivo.1 DHA has also been as…

STAT3 Transcription FactorDocosahexaenoic AcidsCellular differentiationPeroxisome proliferator-activated receptorInflammationSuppressor of Cytokine Signaling ProteinsBiologyEditorials: Cell Cycle FeaturesProinflammatory cytokineMicemedicineAnimalsHumansPhosphorylationPromoter Regions GeneticMolecular BiologyCells Culturedchemistry.chemical_classificationInflammationTumor microenvironmentInterleukin-17TroglitazoneCell DifferentiationCell BiologyPPAR gammaCell Transformation NeoplasticchemistryGene Expression RegulationSuppressor of Cytokine Signaling 3 ProteinImmunologyCancer cellCancer researchTh17 CellsInterleukin 17medicine.symptomDevelopmental Biologymedicine.drugProtein BindingSignal TransductionCell Cycle
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SPARC is a new myeloid-derived suppressor cell marker licensing suppressive activities

2019

Myeloid-derived suppressor cells (MDSC) are well-known key negative regulators of the immune response during tumor growth, however scattered is the knowledge of their capacity to influence and adapt to the different tumor microenvironments and of the markers that identify those capacities. Here we show that the secreted protein acidic and rich in cysteine (SPARC) identifies in both human and mouse MDSC with immune suppressive capacity and pro-tumoral activities including the induction of epithelial-to-mesenchymal transition (EMT) and angiogenesis. In mice the genetic deletion of SPARC reduced MDSC immune suppression and reverted EMT. Sparc−/− MDSC were less suppressive overall and the granu…

STAT3 Transcription Factorlcsh:Immunologic diseases. Allergy0301 basic medicineEpithelial-Mesenchymal TransitionAngiogenesisImmunologyneutrophil extracellular trapsNitric Oxide Synthase Type IIInflammationExtracellular TrapsMice03 medical and health sciences0302 clinical medicineImmune systemBreast cancermedicineMyeloid-derived suppressor cellAnimalsHumansImmunology and AllergyOsteonectinOriginal ResearchMice KnockoutMice Inbred BALB CTumor microenvironmentArginaseChemistryNeutrophilNF-kappa B p50 SubunitSPARCNeutrophil extracellular trapsmyeloid-derived suppressor cells030104 developmental biologyCancer researchMyeloid-derived Suppressor CellTumor necrosis factor alphaSignal transductionmedicine.symptomlcsh:RC581-607Neutrophil extracellular trapBiomarkers030215 immunology
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Induction of tolerogenic lung CD4+ T cells by local treatment with a pSTAT-3 and pSTAT-5 inhibitor ameliorated experimental allergic asthma.

2010

Signal transducer and activator of transcription (STAT)-3 inhibitors play an important role in regulating immune responses. Galiellalactone (GL) is a fungal secondary metabolite known to interfere with the binding of phosphorylated signal transducer and activator of transcription (pSTAT)-3 as well of pSTAT-6 dimers to their target DNA in vitro. Intra nasal delivery of 50 μg GL into the lung of naive Balb/c mice induced FoxP3 expression locally and IL-10 production and IL-12p40 in RNA expression in the airways in vivo. In a murine model of allergic asthma, GL significantly suppressed the cardinal features of asthma, such as airway hyperresponsiveness, eosinophilia and mucus production, after…

STAT3 Transcription Factormedicine.medical_treatmentImmunologyCD11cSuppressor of Cytokine Signaling ProteinsT-Lymphocytes RegulatoryLactonesMiceImmune systemIn vivomedicineSTAT5 Transcription FactorImmunology and AllergyAnimalsIndoleamine-Pyrrole 23-DioxygenaseAnti-Asthmatic AgentsLungAdministration IntranasalCells CulturedMice Inbred BALB CbiologyChemistryFOXP3General MedicineDendritic CellsT-Lymphocytes Helper-Inducerrespiratory systemAsthmaReceptors Interleukin-3CD11c Antigenrespiratory tract diseasesOvalbuminInterleukin 10CytokineSuppressor of Cytokine Signaling 3 ProteinImmunologySTAT proteinCancer researchbiology.proteinFemaleInterleukin-4T-Box Domain Proteins
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The YJL185C, YLR376C and YJR129C genes of Saccharomyces cerevisiae are probably involved in regulation of the glyoxylate cycle

2006

The ER24 aci (acidification) mutant of Saccharomyces cerevisiae excreting protons in the absence of glucose was transformed with a multicopy yeast DNA plasmid library. Three different DNA fragments restored the wild-type phenotype termed Aci- because it does not acidify the complete glucose medium under the tested conditions. Molecular dissection of the transforming DNA fragments identified two multicopy suppressor genes YJL185C, YJR129C and one allelic YLR376C. Disruption of either of the three genes in wild-type yeast strain resulted in acidification of the medium (Aci+ phenotype) similarly to the original ER24 mutant. These data indicate the contribution of the ER24 gene product Ylr376Cp…

Saccharomyces cerevisiae ProteinsMutantSaccharomyces cerevisiaeGenes FungalGlyoxylate cycleAutophagy-Related ProteinsGlyoxylatesMethyltransferasesSaccharomyces cerevisiaeBiologyHydrogen-Ion Concentrationbiology.organism_classificationGeneral Biochemistry Genetics and Molecular BiologyYeastCulture MediaGene productchemistry.chemical_compoundPlasmidchemistryBiochemistryGenes SuppressorGeneDNAMetabolic Networks and Pathways
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DNA damage causes TP53-dependent coupling of self-renewal and senescence pathways in embryonal carcinoma cells.

2013

Recent studies have highlighted an apparently paradoxical link between self-renewal and senescence triggered by DNA damage in certain cell types. In addition, the finding that TP53 can suppress senescence has caused a re-evaluation of its functional role in regulating these outcomes. To investigate these phenomena and their relationship to pluripotency and senescence, we examined the response of the TP53-competent embryonal carcinoma (EC) cell line PA-1 to etoposide-induced DNA damage. Nuclear POU5F1/OCT4A and P21CIP1 were upregulated in the same cells following etoposide-induced G 2M arrest. However, while accumulating in the karyosol, the amount of OCT4A was reduced in the chromatin fract…

SenescenceCyclin-Dependent Kinase Inhibitor p21OCT4A/POU5F1Embryonal Carcinoma Stem CellssenescenceDNA RepairDNA repairDNA damagetumor cellsBiologyProtein Serine-Threonine Kinasesself-renewalHistonesAurora KinasesCell Line TumorReportAutophagyAurora Kinase BHumansTP53PhosphorylationRNA Small InterferingMolecular BiologyMitosisCellular SenescenceCyclin-Dependent Kinase Inhibitor p16EtoposideOvarian NeoplasmsEmbryonal Carcinoma Stem CellsCell BiologyG2-M DNA damage checkpointbeta-GalactosidasepluripotencyAntineoplastic Agents PhytogenicChromatinUp-RegulationG2 Phase Cell Cycle CheckpointsCheckpoint Kinase 2Cancer researchDNA damageFemaleRNA InterferenceRad51 RecombinaseTumor Suppressor Protein p53Cell agingOctamer Transcription Factor-3Developmental BiologyCell cycle (Georgetown, Tex.)
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The dual role of p53: DNA protection and antioxidant.

2011

The classical functions of p53 protein are those related to its role on DNA damage, cell growth arrest, senescence and apoptosis. For this reason it is called 'the guardian of the genome' and is considered one of the most important players in the development of cancer. However, more recently it has been show that p53 is not only involved in cancer, but also in ageing. p53 is stimulated by stress, which in turn results in the activation of a wide range of transcriptional targets. Low-intensity stress will activate p53 in a manner which results in antioxidant response, thus protecting against ageing because of its antioxidant function. On the contrary, high-intensity activation of p53 will re…

SenescenceGenome instabilityDNA protectionAgingDNA damageBiologymedicine.disease_causeBiochemistryAntioxidantsGenomic InstabilityNeoplasmsmedicineAnimalsHumansCellular SenescenceHeat-Shock ProteinsCell growthCell CycleGeneral MedicineCell cycleCell biologyBiochemistryAgeingTumor Suppressor Protein p53Reactive Oxygen SpeciesOxidative stressFree radical research
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