Search results for "interference"

showing 10 items of 573 documents

CD36 is involved in lycopene and lutein uptake by adipocytes and adipose tissue cultures

2011

International audience; Scope: Carotenoids are mainly stored in adipose tissue. However, nothing is known regarding the uptake of carotenoids by adipocytes. Thus, our study explored the mechanism by which lycopene and lutein, two major human plasma carotenoids, are transported. Methods and results: CD36 was a putative candidate for this uptake, 3T3-L1 cells were treated with sulfosuccinimidyl oleate, a CD36-specific inhibitor. sulfosuccinimidyl oleate-treated cells showed a significant decrease in both lycopene and lutein uptake as compared to control cells. Their uptake was also decreased by partial inhibition of CD36 expression using siRNA, whereas the overexpression of CD36 in Cos-1 cell…

CD36 AntigensMaleLutein030309 nutrition & dieteticsCD36[ SDV.AEN ] Life Sciences [q-bio]/Food and NutritionLYCOPENEAdipose tissueOleic Acidschemistry.chemical_compoundMiceChlorocebus aethiopsRNA Small InterferingCAROTENOIDSCarotenoidComputingMilieux_MISCELLANEOUSchemistry.chemical_classificationMice KnockoutGENE CD360303 health sciencesbiologyCD 36food and beveragesLycopene3. Good healthADIPOCYTESADIPOSE TISSUEBiochemistryCOS CellsRNA InterferenceBiotechnologyAdipose tissue macrophagesAdipose Tissue WhiteSuccinimides03 medical and health sciencesOrgan Culture Techniques3T3-L1 CellsTRANSPORTEUR BIOLOGIQUEparasitic diseasesAnimalsHumans030304 developmental biologyBiological Transport[SDV.AEN] Life Sciences [q-bio]/Food and NutritionGLYCOPROTEINRchemistryLUTEINbiology.protein[SDV.AEN]Life Sciences [q-bio]/Food and NutritionEx vivoFood ScienceExplant culture
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SOCS3 transactivation by PPARγ prevents IL-17-driven cancer growth.

2013

Abstract Activation of the transcription factor PPARγ by the n-3 fatty acid docosahexaenoic acid (DHA) is implicated in controlling proinflammatory cytokine secretion, but the intracellular signaling pathways engaged by PPARγ are incompletely characterized. Here, we identify the adapter-encoding gene SOCS3 as a critical transcriptional target of PPARγ. SOCS3 promoter binding and gene transactivation by PPARγ was associated with a repression in differentiation of proinflammatory T-helper (TH)17 cells. Accordingly, TH17 cells induced in vitro displayed increased SOCS3 expression and diminished capacity to produce interleukin (IL)-17 following activation of PPARγ by DHA. Furthermore, naïve CD4…

CD4-Positive T-LymphocytesCancer ResearchAngiogenesisMammary Neoplasms Experimental/genetics/pathology/prevention & controlSuppressor of Cytokine Signaling Proteinsddc:616.07BioinformaticsTransactivationMice0302 clinical medicineTumor Burden/drug effects/geneticsSOCS3Docosahexaenoic Acids/administration & dosage/pharmacologyPromoter Regions GeneticMice Knockout0303 health sciencesMice Inbred BALB CChemistryReverse Transcriptase Polymerase Chain ReactionInterleukin-17InterleukinCell DifferentiationCell biologyTumor BurdenOncology030220 oncology & carcinogenesisFemaleRNA InterferenceInterleukin 17Th17 Cells/drug effects/metabolismTranscriptional ActivationDocosahexaenoic AcidsBlotting WesternMice NudeCD4-Positive T-Lymphocytes/drug effects/metabolismProinflammatory cytokine03 medical and health sciencesSuppressor of Cytokine Signaling Proteins/genetics/metabolismCell Line TumorAnimalsTranscription factor030304 developmental biologyMammary Neoplasms ExperimentalPromoter Regions Genetic/geneticsDietMice Inbred C57BLPPAR gammaInterleukin-17/metabolismCell cultureSuppressor of Cytokine Signaling 3 ProteinCell Differentiation/drug effectsPPAR gamma/agonists/genetics/metabolismTh17 CellsCancer research
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Shaping of a ground state rotational wavepacket by frequency-chirped pulses

2001

0953-4075; A coherent rotational superposition state is produced in the ground vibronic level of N2 through the interaction of the molecule with the electric field vector of a nonresonant laser pulse. This rotational wavepacket is shaped with a linear frequency chirp of the laser field. The structural shape of the rotational coherences shows a strong dependence with the frequency-chirp amplitude. A comparison with a theoretical model allows the interpretation of the observed effects in terms of dephasing of the wavepacket induced by the laser phase distortion. Application of the presented results to the phase characterization of short XUV pulses is suggested.

CONTROLDephasingPhase (waves)Physics::Opticslaw.inventionCOHERENTSuperposition principleINDUCED POLARIZATION SPECTROSCOPYlawPhysics::Atomic and Molecular ClustersChirpPhysics::Atomic PhysicsFIELDFEMTOSECOND LASER-PULSESINTERFERENCEPhysicsPhase distortionPHOTODISSOCIATIONCondensed Matter PhysicsLaserEVOLUTIONN-2Atomic and Molecular Physics and OpticsAmplitudeAtomic physicsGround stateJournal of Physics B: Atomic, Molecular and Optical Physics
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MYCN sensitizes human neuroblastoma to apoptosis by HIPK2 activation through a DNA damage response.

2010

Abstract MYCN amplification occurs in approximately 20% of human neuroblastomas and is associated with early tumor progression and poor outcome, despite intensive multimodal treatment. However, MYCN overexpression also sensitizes neuroblastoma cells to apoptosis. Thus, uncovering the molecular mechanisms linking MYCN to apoptosis might contribute to designing more efficient therapies for MYCN-amplified tumors. Here we show that MYCN-dependent sensitization to apoptosis requires activation of p53 and its phosphorylation at serine 46. The p53S46 kinase HIPK2 accumulates on MYCN expression, and its depletion by RNA interference impairs p53S46 phosphorylation and apoptosis. Remarkably, MYCN ind…

Cancer ResearchApoptosisCell Cycle ProteinsAtaxia Telangiectasia Mutated ProteinsProtein-Serine-Threonine KinaseAtaxia Telangiectasia Mutated ProteinNeuroblastomaCell Cycle ProteinSerinePhosphorylationNuclear ProteinOncogene Proteinseducation.field_of_studyN-Myc Proto-Oncogene ProteinAntibiotics AntineoplasticKinaseOncogene ProteinNuclear ProteinsDNA-Binding ProteinsOncologyPhosphorylationRNA InterferenceHumanDNA damageDNA-Binding ProteinPopulationBlotting WesternBiologyProtein Serine-Threonine KinasesN-Myc Proto-Oncogene ProteinBleomycinNeuroblastomaCell Line TumormedicineHumanseducationneoplasmsMolecular BiologyTumor Suppressor ProteinTumor Suppressor ProteinsApoptosimedicine.diseaseTumor progressionApoptosisMutationCancer researchTumor Suppressor Protein p53Carrier ProteinCarrier ProteinsDNA DamageMolecular cancer research : MCR
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Suppression of Mcl-1 via RNA interference sensitizes human hepatocellular carcinoma cells towards apoptosis induction

2006

Abstract Background Hepatocelluar carcinoma (HCC) is one of the most common cancers worldwide and a major cause of cancer-related mortality. HCC is highly resistant to currently available chemotherapeutic drugs. Defects in apoptosis signaling contribute to this resistance. Myeloid cell leukemia-1 (Mcl-1) is an anti-apoptotic member of the Bcl-2 protein family which interferes with mitochondrial activation. In a previous study we have shown that Mcl-1 is highly expressed in tissues of human HCC. In this study, we manipulated expression of the Mcl-1 protein in HCC cells by RNA interference and analyzed its impact on apoptosis sensitivity of HCC cells in vitro. Methods RNA interference was per…

Cancer ResearchCarcinoma HepatocellularMyeloidCellAntineoplastic AgentsApoptosisBiologylcsh:RC254-282RNA interferenceCell Line Tumorhemic and lymphatic diseasesGeneticsmedicineHumansneoplasmsLiver Neoplasmslcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseasedigestive system diseasesIn vitroNeoplasm ProteinsGene Expression Regulation NeoplasticLeukemiamedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2OncologyApoptosisHepatocellular carcinomaCancer researchMyeloid Cell Leukemia Sequence 1 ProteinRNA InterferenceStem cellResearch ArticleBMC Cancer
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IL1β Induces Mesenchymal Stem Cells Migration and Leucocyte Chemotaxis Through NF-κB

2012

Mesenchymal stem cells are often transplanted into inflammatory environments where they are able to survive and modulate host immune responses through a poorly understood mechanism. In this paper we analyzed the responses of MSC to IL-1β: a representative inflammatory mediator. Microarray analysis of MSC treated with IL-1β revealed that this cytokine activateds a set of genes related to biological processes such as cell survival, cell migration, cell adhesion, chemokine production, induction of angiogenesis and modulation of the immune response. Further more detailed analysis by real-time PCR and functional assays revealed that IL-1β mainly increaseds the production of chemokines such as CC…

Cancer ResearchChemokineMigration and adhesionmedicine.medical_treatmentInterleukin-1betaBiologyArticleInterleukin 1βExtracellular matrixCell MovementCell AdhesionLeukocytesmedicineHumansCell adhesionCell ProliferationOligonucleotide Array Sequence AnalysisCell adhesion moleculeGene Expression ProfilingChemotaxisNF-kappa BMesenchymal Stem CellsCell migrationCell BiologyFibronectinsI-kappa B KinaseCell biologyChemotaxis LeukocyteHEK293 CellsCXCL3CytokineGene Knockdown Techniquesbiology.proteinIntercellular Signaling Peptides and ProteinsRNA InterferenceCollagenLamininChemokinesInflammation MediatorsStem cellSignal TransductionDevelopmental BiologyStem Cell Reviews and Reports
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Efficacy of BET Bromodomain Inhibition in Kras-Mutant Non–Small Cell Lung Cancer

2013

Abstract Purpose: Amplification of MYC is one of the most common genetic alterations in lung cancer, contributing to a myriad of phenotypes associated with growth, invasion, and drug resistance. Murine genetics has established both the centrality of somatic alterations of Kras in lung cancer, as well as the dependency of mutant Kras tumors on MYC function. Unfortunately, drug-like small-molecule inhibitors of KRAS and MYC have yet to be realized. The recent discovery, in hematologic malignancies, that bromodomain and extra-terminal (BET) bromodomain inhibition impairs MYC expression and MYC transcriptional function established the rationale of targeting KRAS-driven non–small cell lung cance…

Cancer ResearchLKB1Lung NeoplasmsMutantApoptosisMYCAMP-Activated Protein KinasesProtein Serine-Threonine KinasesBiologyNSCLCmedicine.disease_causeArticleProto-Oncogene Proteins c-mycProto-Oncogene Proteins p21(ras)MiceRNA interferenceCarcinoma Non-Small-Cell LungCell Line TumorKRASmedicineAnimalsRNA Small InterferingLung cancerneoplasmsCell ProliferationMice KnockoutGene knockdownCell growthNuclear ProteinsCancerAzepinesTriazolesBETmedicine.diseaseMolecular biologydigestive system diseasesrespiratory tract diseasesBromodomainOncologyCancer researchRNA InterferenceKRASSignal TransductionTranscription FactorsClinical Cancer Research
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Molecular mechanisms of HLA class I antigen abnormalities following viral infection and transformation.

2005

In humans as in other animal species, CD8+ cytotoxic T lymphocytes (CTLs) play an important if not the major role in controlling virus-infected and malignant cell growth. The interactions between CD8+ T cells and target cells are mediated by human leukocyte antigen (HLA) class I antigens loaded with viral and tumor antigen-derived peptides along with costimulatory receptor/ligand stimuli. Thus, to escape from CD8+ T-cell recognition and destruction, viruses and tumor cells have developed strategies to inhibit the expression and/or function of HLA class I antigens. In contrast, cells with downregulated MHC class I surface expression can be recognized by NK cells, although NK cell-mediated ly…

Cancer ResearchMacromolecular SubstancesDown-RegulationGenes MHC Class IHuman leukocyte antigenCD8-Positive T-LymphocytesNatural killer cellAntigenHLA AntigensNeoplasmsMHC class IViral InterferencemedicineCytotoxic T cellHumansAntigen-presenting cellbiologyMHC class I antigenAntigen processingmedicine.anatomical_structureOncologyVirus DiseasesImmunologybiology.proteinImmunotherapySignal TransductionInternational journal of cancer
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PDGFRβ and FGFR2 mediate endothelial cell differentiation capability of triple negative breast carcinoma cells

2014

Triple negative breast cancer (TNBC) is a very aggressive subgroup of breast carcinoma, still lacking specific markers for an effective targeted therapy and with a poorer prognosis compared to other breast cancer subtypes. In this study we investigated the possibility that TNBC cells contribute to the establishment of tumor vascular network by the process known as vasculogenic mimicry, through endothelial cell differentiation. Vascular-like functional properties of breast cancer cell lines were investigated in vitro by tube formation assay and in vivo by confocal microscopy, immunofluorescence or immunohistochemistry on frozen tumor sections. TNBCs express endothelial markers and acquire th…

Cancer ResearchPathologymedicine.medical_specialtyPDGFRmedicine.medical_treatmentTriple Negative Breast NeoplasmsMice SCIDBiologyEndothelial cell differentiationTargeted therapyReceptor Platelet-Derived Growth Factor betachemistry.chemical_compoundBreast cancerCell Line TumorGeneticsmedicineAnimalsHumansVasculogenic mimicryBreastRNA Small InterferingReceptor Fibroblast Growth Factor Type 2skin and connective tissue diseasesTriple-negative breast cancerResearch ArticlesNeovascularization PathologicFGFREndothelial CellsCell DifferentiationGeneral MedicineTriple Negative Breast Neoplasmsmedicine.diseaseImmunohistochemistryVascular endothelial growth factorOncologychemistryVasculogenic mimicryCancer researchMolecular MedicineTNBC; Vasculogenic mimicry; PDGFR; FGFRTriple-Negative Breast CarcinomaFemaleRNA InterferenceTNBC
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Aurora-A Transcriptional Silencing and Vincristine Treatment Show a Synergistic Effect in Human Tumor Cells

2008

Aurora-A is a centrosome-associated serine/threonine kinase that is overexpressed in multiple types of human tumors. Primarily, Aurora-A functions in centrosome maturation and mitotic spindle assembly. Overexpression of Aurora-A induces centrosome amplification and G 2 /M cell cycle progression. Recently, it was observed that overexpression of Aurora-A renders cells resistant to cisplatin (CDDP)-, etoposide-, and paclitaxel-induced apoptosis.Our results indicate that already in initial stages of cancer progression Aurora-A overexpression could have a major role in inducing supernumerary centrosomes and aneuploidy, as shown by immunohistochemistry on tissue sections from various stages of hu…

Cancer ResearchPathologymedicine.medical_specialtyTranscription GeneticApoptosismacromolecular substancesProtein Serine-Threonine KinasesBiologyTransfectionPLK1Aurora KinasesRNA interferenceCell Line TumormedicineHumansGene silencingGene SilencingRNA Small InterferingMitotic catastropheCentrosomeCisplatinCarcinomaCell CycleDrug SynergismAuroraA/stk15centrosome amplificationAneuploidy CINGeneral MedicineCell cycleAneuploidyAntineoplastic Agents PhytogenicGene Expression Regulation NeoplasticSettore BIO/18 - Geneticaenzymes and coenzymes (carbohydrates)OncologyVincristineCentrosomeColonic Neoplasmsembryonic structuresCancer cellCancer researchbiological phenomena cell phenomena and immunityHeLa Cellsmedicine.drugOncology Research Featuring Preclinical and Clinical Cancer Therapeutics
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