Search results for " Small Interfering"

showing 10 items of 211 documents

Involvement of PAR-4 in Cannabinoid-Dependent Sensitization of Osteosarcoma Cells to TRAIL-Induced Apoptosis

2014

The synthetic cannabinoid WIN 55,212-2 is a potent cannabinoid receptor agonist with anticancer potential. Experiments were performed to determine the effects of WIN on proliferation, cell cycle distribution, and programmed cell death in human osteosarcoma MG63 and Saos-2 cells. Results show that WIN induced G2/M cell cycle arrest, which was associated with the induction of the main markers of ER stress (GRP78, CHOP and TRB3). In treated cells we also observed the conversion of the cytosolic form of the autophagosome marker LC3-I into LC3-II (the lipidated form located on the autophagosome membrane) and the enhanced incorporation of monodansylcadaverine and acridine orange, two markers of t…

AutophagosomeautophagyProgrammed cell deathCannabinoids ER stress autophagy TRAIL osteosarcoma cells GRP78/PAR-4 complex.Cannabinoid receptorMorpholinesCellApoptosisTRAILNaphthalenesBiologyGRP78/PAR-4 complex.Applied Microbiology and BiotechnologyTNF-Related Apoptosis-Inducing LigandCadaverineCell Line TumorSettore BIO/10 - BiochimicamedicineHumansRNA Small InterferingEndoplasmic Reticulum Chaperone BiPMolecular BiologyHeat-Shock ProteinsEcology Evolution Behavior and SystematicsCell ProliferationCannabinoid Receptor AgonistsOsteosarcomaCannabinoidsAutophagyCell Cycle Checkpointsosteosarcoma cellsCell BiologyCell cycleEndoplasmic Reticulum StressAcridine OrangeBenzoxazinesCell biologymedicine.anatomical_structureApoptosisAutophagosome membraneApoptosis Regulatory ProteinsER stressMicrotubule-Associated ProteinsResearch PaperDevelopmental Biology
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Recent advances in smart biotechnology: Hydrogels and nanocarriers for tailored bioactive molecules depot

2017

Over the past ten years, the global biopharmaceutical market has remarkably grown, with ten over the top twenty worldwide high performance medical treatment sales being biologics. Thus, biotech R&D (research and development) sector is becoming a key leading branch, with expanding revenues. Biotechnology offers considerable advantages compared to traditional therapeutic approaches, such as reducing side effects, specific treatments, higher patient compliance and therefore more effective treatments leading to lower healthcare costs. Within this sector, smart nanotechnology and colloidal self-assembling systems represent pivotal tools able to modulate the delivery of therapeutics. A comprehens…

Bioactive molecules02 engineering and technologyHepatocellular-carcinoma cells01 natural sciencesMiceColloid and Surface ChemistryDrug Delivery SystemsCarbon nano materialNanotechnologyMolecular Targeted TherapyTransgenesRNA Small InterferingPatient complianceTransfer radical polymerizationMicro/nanocarrierMedical treatmentMicro/nanocarriersBioactive molecule deliveryHydrogelsSurfaces and Interfaces021001 nanoscience & nanotechnologyLiposomeBiopharmaceuticalOral deliverySelf-healing hydrogelsIntercellular Signaling Peptides and Proteins0210 nano-technologyAssembling peptide hydrogelsSurfaces and InterfaceNucleic-acid deliveryPlasmidsDiagnostic ImagingSolid lipid nanoparticlesNanotechnology010402 general chemistryAntibodiesSmall Molecule LibrariesCarbon nano-onionsIn-vivoAnimalsHumansPhysical and Theoretical Chemistrybusiness.industryDrug-delivery0104 chemical sciencesBiotechnologyHydrogelSettore CHIM/09 - Farmaceutico Tecnologico ApplicativoMolecular ProbesBioactive molecule delivery; Carbon nano materials; Hydrogels; Liposomes; Micro/nanocarriers; Surfaces and Interfaces; Physical and Theoretical Chemistry; Colloid and Surface ChemistryLiposomesNonviral gene deliveryCarbon nano materialsNanoparticlesBusinessNanocarriers
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Meox2/Tcf15 Heterodimers Program the Heart Capillary Endothelium for Cardiac Fatty Acid Uptake

2015

Background— Microvascular endothelium in different organs is specialized to fulfill the particular needs of parenchymal cells. However, specific information about heart capillary endothelial cells (ECs) is lacking. Methods and Results— Using microarray profiling on freshly isolated ECs from heart, brain, and liver, we revealed a genetic signature for microvascular heart ECs and identified Meox2/Tcf15 heterodimers as novel transcriptional determinants. This signature was largely shared with skeletal muscle and adipose tissue endothelium and was enriched in genes encoding fatty acid (FA) transport–related proteins. Using gain- and loss-of-function approaches, we showed that Meox2/Tcf15 media…

CD36 AntigensHeterozygoteEndotheliumCD36Cardiac Output LowAdipose tissueLipoproteins VLDLBiologyFatty Acid-Binding ProteinsMicePhysiology (medical)Protein Interaction MappingBasic Helix-Loop-Helix Transcription FactorsmedicineAnimalsHumansRNA Small InterferingTranscription factorCells CulturedHomeodomain Proteinschemistry.chemical_classificationLipoprotein lipaseMyocardiumFatty AcidsEndothelial CellsFatty acidSkeletal muscleMetabolismCoronary VesselsCell biologyMice Inbred C57BLLipoprotein LipaseGlucosemedicine.anatomical_structureAdipose TissuechemistryBiochemistryTissue Array Analysisbiology.proteinTranscriptomeCardiology and Cardiovascular MedicineCirculation
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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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MS4A12 is a colon-selective store-operated calcium channel promoting malignant cell processes.

2008

AbstractUsing a data mining approach for the discovery of new targets for antibody therapy of colon cancer, we identified MS4A12, a sequence homologue of CD20. We show that MS4A12 is a cell surface protein. Expression analysis and immunohistochemistry revealed MS4A12 to be a colonic epithelial cell lineage gene confined to the apical membrane of colonocytes with strict transcriptional repression in all other normal tissue types. Expression is maintained upon malignant transformation in 63% of colon cancers. Ca2+ flux analyses disclosed that MS4A12 is a novel component of store-operated Ca2+ entry in intestinal cells. Using RNAi-mediated gene silencing, we show that loss of MS4A12 in LoVo co…

Calcium Channel Blockers/pharmacologyCancer ResearchColorectal cancerColonCalcium Channels/geneticsCell Differentiation/geneticsEpidermal Growth Factor/pharmacologyBiologyRNA Small Interfering/pharmacologyModels BiologicalMalignant transformationEpidermal growth factorCell Line TumormedicineMembrane Proteins/antagonists & inhibitorsHumansGrowth factor receptor inhibitorNeoplasm InvasivenessRNA Small InterferingEpidermal Growth FactorGene Expression ProfilingMembrane ProteinsColonic Neoplasms/geneticsCell DifferentiationApical membranemedicine.diseaseCalcium Channel BlockersColon/metabolismCell biologyChemokines/metabolismProtein Structure TertiaryGene Expression Regulation NeoplasticOncologyCell cultureOrgan SpecificityCancer cellColonic NeoplasmsDisease ProgressionCalcium ChannelsChemokinesA431 cellsCancer research
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TCDD deregulates contact inhibition in rat liver oval cells via Ah receptor, JunD and cyclin A.

2007

The aryl hydrocarbon receptor (AhR) is a transcription factor involved in physiological processes, but also mediates most, if not all, toxic responses to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Activation of the AhR by TCDD leads to its dimerization with aryl hydrocarbon nuclear translocator (ARNT) and transcriptional activation of several phase I and II metabolizing enzymes. However, this classical signalling pathway so far failed to explain the pleiotropic hazardous effects of TCDD, such as developmental toxicity and tumour promotion. Thus, there is an urgent need to define genetic programmes orchestrated by AhR to unravel its role in physiology and toxicology. Here we show that TCDD …

Cancer ResearchAryl hydrocarbon receptor nuclear translocatorPolychlorinated Dibenzodioxinscyclin AProto-Oncogene Proteins c-junCyclin DCyclin Acell cycle controlCyclin ATetrachlorodibenzodioxinModels BiologicalDownregulation and upregulationGeneticsAnimalsRNA Small InterferingMolecular BiologyTranscription factorAryl hydrocarbon receptorCells CulturedbiologyContact InhibitionContact inhibitionCell cycleAryl hydrocarbon receptorRatsAdult Stem CellsLiverReceptors Aryl Hydrocarbonliver oval cellsbiology.proteinCancer researchJunDOncogene
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Novel pathway in Bcr-Abl signal transduction involves Akt-independent, PLC-γ1-driven activation of mTOR/p70S6-kinase pathway

2009

In chronic myeloid leukemia, activation of the phosphoinositide 3-kinase (PI3K)/Akt pathway is crucial for survival and proliferation of leukemic cells. Essential downstream molecules involve mammalian target of rapamycin (mTOR) and S6-kinase. Here, we present a comprehensive analysis of the molecular events involved in activation of these key signaling pathways. We provide evidence for a previously unrecognized phospholipase C-gamma1 (PLC-gamma1)-controlled mechanism of mTOR/p70S6-kinase activation, which operates in parallel to the classical Akt-dependent machinery. Short-term imatinib treatment of Bcr-Abl-positive cells caused dephosphorylation of p70S6-K and S6-protein without inactivat…

Cancer ResearchBlotting WesternMedizinFusion Proteins bcr-ablApoptosisProtein Serine-Threonine KinasesBiologyPiperazinesMiceLeukemia Myelogenous Chronic BCR-ABL Positivehemic and lymphatic diseasesGeneticsAnimalsHumansRNA Small InterferingProtein Kinase InhibitorsMolecular BiologyProtein kinase BCAMKPI3K/AKT/mTOR pathwayPhospholipase C gammaCell growthKinaseTOR Serine-Threonine KinasesRPTORIntracellular Signaling Peptides and ProteinsRibosomal Protein S6 Kinases 70-kDaCell biologyEnzyme ActivationPyrimidinesBenzamidesembryonic structuresImatinib MesylateCancer researchPhosphorylationSignal transductionProto-Oncogene Proteins c-aktSignal TransductionOncogene
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A placenta-specific gene ectopically activated in many human cancers is essentially involved in malignant cell processes.

2007

Abstract The identification and functional characterization of tumor-specific genes is a prerequisite for the development of targeted cancer therapies. Using an integrated data mining and experimental validation approach for the discovery of new targets for antibody therapy of cancer, we identified PLAC1. PLAC1 is a placenta-specific gene with no detectable expression in any other normal human tissue. However, it is frequently aberrantly activated and highly expressed in a variety of tumor types, in particular breast cancer. RNAi-mediated silencing of PLAC1 in MCF-7 and BT-549 breast cancer cells profoundly impairs motility, migration, and invasion and induces a G1-S cell cycle block with n…

Cancer ResearchGene knockdownbiologyCell CycleCancerBreast NeoplasmsCell cyclePregnancy Proteinsmedicine.diseaseGene Expression Regulation NeoplasticCyclin D1Breast cancerCell Transformation NeoplasticOncologyCell MovementCell Line TumorCancer cellImmunologybiology.proteinCancer researchmedicineGene silencingHumansAntibodyRNA Small InterferingCancer research
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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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Role of SHP2 for FLT3-dependent proliferation and transformation in 32D cells.

2008

Fms-like tyrosine kinase 3 (FLT3) is a class III receptor tyrosine kinase, which plays a role in proliferation and differentiation of B-cell progenitors, myelomonocytic and dendritic cells, as well as in the maintenance of pluripotent hematopoietic stem cells (reviewed in Stirewalt and Radich,1and Schmidt-Arras et al.2). Recently, FLT3 has received much attention as an important oncoprotein. Mutations in FLT3 that lead to constitutive activation are among the most common molecular lesions found in acute myeloid leukemia.3 The most prevalent type of mutations result in internal tandem duplications (ITD) of amino-acid stretches in the juxtamembrane domain of FLT3. FLT3-ITD is constitutively a…

Cancer ResearchMyeloidProtein Tyrosine Phosphatase Non-Receptor Type 11Biologymedicine.disease_causeReceptor tyrosine kinaseCell LineMicefluids and secretionshemic and lymphatic diseasesmedicineAnimalsHumansRNA Small InterferingCell ProliferationMice Inbred C3Hhemic and immune systemsHematologyHaematopoiesismedicine.anatomical_structureCell Transformation NeoplasticOncologyfms-Like Tyrosine Kinase 3Trk receptorembryonic structuresCancer researchbiology.proteinStem cellSignal transductionCarcinogenesisTyrosine kinaseSignal TransductionLeukemia
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