Search results for " EXPRESSION"

showing 10 items of 4731 documents

Targeting Bcl-2 family proteins modulates the sensitivity of B-cell lymphoma to rituximab-induced apoptosis.

2008

The chimeric monoclonal antibody rituximab is the standard of care for patients with B-cell non-Hodgkin lymphoma (B-NHL). Rituximab mediates complementdependent cytotoxicity and antibodydependent cellular cytotoxicity of CD20-positive human B cells. In addition, rituximab sensitizes B-NHL cells to cytotoxic chemotherapy and has direct apoptotic and antiproliferative effects. Whereas expression of the CD20 antigen is a natural prerequisite for rituximab sensitivity, cell-autonomous factors determining the response of B-NHL to rituximab are less defined. To this end, we have studied rituximab-induced apoptosis in human B-NHL models. We find that rituximab directly triggers apoptosis via the m…

Programmed cell deathLymphoma B-CellImmunologyMedizinAntineoplastic AgentsApoptosisMice SCIDBiochemistryPiperazinesNitrophenolsAntibodies Monoclonal Murine-DerivedMicePhosphatidylinositol 3-Kinasesimmune system diseaseshemic and lymphatic diseasesCell Line TumormedicineAnimalsHumansB-cell lymphomaCD20SulfonamidesbiologyBcl-2 familyBiphenyl CompoundsAntibodies MonoclonalCell BiologyHematologymedicine.diseaseAntigens CD20LymphomaGene Expression Regulation NeoplasticProto-Oncogene Proteins c-bcl-2Apoptosisbiology.proteinCancer researchMyeloid Cell Leukemia Sequence 1 ProteinRituximabSignal transductionRituximabNeoplasm Transplantationmedicine.drugSignal TransductionBlood
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Parthenolide induces caspase-independent and AIF-mediated cell death in human osteosarcoma and melanoma cells

2013

The mechanism of the cytotoxic effect exerted by parthenolide on tumor cells is not clearly defined today. This article shows that parthenolide stimulates in human osteosarcoma MG63 and melanoma SK-MEL-28 cells a mechanism of cell death, which is not prevented by z-VAD-fmk and other caspase inhibitors. In particular treatment with parthenolide rapidly stimulated (1-2 h) reactive oxygen species (ROS) generation by inducing activation of extracellular signal-regulated kinase 1/2 (ERK 1/2) and NADPH oxidase. This event caused depletion of thiol groups and glutathione, NF-κB inhibition, c-Jun N-terminal kinase (JNK) activation, cell detachment from the matrix, and cellular shrinkage. The increa…

Programmed cell deathMAP Kinase Signaling SystemPhysiologyClinical BiochemistryAmino Acid Chloromethyl Ketoneschemistry.chemical_compoundCell Line TumorSettore BIO/10 - BiochimicaHumansParthenolidePropidium iodideFragmentation (cell biology)MelanomaCaspaseOsteosarcomaCell DeathbiologyNF-kappa BApoptosis Inducing FactorNADPH OxidasesCell BiologyCaspase InhibitorsCell biologyGene Expression Regulation NeoplasticchemistryApoptosisCell cultureCaspasesbiology.proteinApoptosis-inducing factorReactive Oxygen SpeciesSesquiterpenesParthenolide caspase-independent cell death ROS AIFJournal of Cellular Physiology
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ROS-Dependent ER Stress and Autophagy Mediate the Anti-Tumor Effects of Tributyltin (IV) Ferulate in Colon Cancer Cells

2020

Organotin compounds represent potential cancer therapeutics due to their pro-apoptotic action. We recently synthesized the novel organotin ferulic acid derivative tributyltin (IV) ferulate (TBT-F) and demonstrated that it displays anti-tumor properties in colon cancer cells related with autophagic cell death. The purpose of the present study was to elucidate the mechanism of TBT-F action in colon cancer cells. We specifically show that TBT-F-dependent autophagy is determined by a rapid generation of reactive oxygen species (ROS) and correlated with endoplasmic reticulum (ER) stress. TBT-F evoked nuclear factor erythroid-2 related factor 2 (Nrf2)-mediated antioxidant response and Nrf2 silenc…

Programmed cell deathNF-E2-Related Factor 2Glucose-regulated proteinApoptosismedicine.disease_causeArticleCatalysisInorganic Chemistrylcsh:ChemistrySettore BIO/10 - BiochimicaAutophagyTumor Cells CulturedmedicineHumansGene silencingoxidative stressPhysical and Theoretical ChemistryEndoplasmic Reticulum Chaperone BiPMolecular Biologylcsh:QH301-705.5tributyltin (IV) derivativeSpectroscopyCell Proliferationoxidative strebiologyChemistryEndoplasmic reticulumOrganic ChemistryAutophagyCancerROSGeneral Medicineendoplasmic reticulum stremedicine.diseaseComputer Science ApplicationsGene Expression Regulation Neoplasticlcsh:Biology (General)lcsh:QD1-999autophagic cell deathColonic NeoplasmsUnfolded protein responseCancer researchbiology.proteinendoplasmic reticulum stressTrialkyltin CompoundsReactive Oxygen SpeciesOxidative stress
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Dexamethasone treatment of naïve organ of Corti explants alters the expression pattern of apoptosis-related genes.

2009

Dexamethasone treatment of organ of Corti explants challenged with an ototoxic level of an inflammatory cytokine modulates NFkappaB signaling and the expression levels of both pro-and anti-apoptosis-related genes. It is not known if naïve organ of Corti explants will respond in a similar manner to treatment with a corticosteroid. This study examines the response of naïve organ of Corti explants to treatment with dexamethasone.Three-day-old rat organ of Corti explants were cultured for 1, 2, or 4 days. Four-day in vitro cultures were fixed, stained with FITC-phalloidin and hair cells were counted. ELISA was performed on 2-day cultures to determine the levels of phosphorylated nuclear factor …

Programmed cell deathPathologymedicine.medical_specialtyTime Factorsmedicine.medical_treatmentAnti-Inflammatory Agentsbcl-X ProteinGene ExpressionApoptosisCell CountEnzyme-Linked Immunosorbent AssayBiologyDexamethasoneStatistics NonparametricAndrologyRats Sprague-DawleyOrgan Culture TechniquesGene expressionmedicineAnimalsInner earPhosphorylationMolecular BiologyOrgan of CortiDexamethasonebcl-2-Associated X ProteinAnalysis of VarianceReverse Transcriptase Polymerase Chain ReactionGeneral NeuroscienceNF-kappa BRatsCytokinemedicine.anatomical_structureAnimals NewbornProto-Oncogene Proteins c-bcl-2Organ of CortiApoptosisReceptors Tumor Necrosis Factor Type Isense organsNeurology (clinical)Hair cellDevelopmental Biologymedicine.drugBrain research
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Calcium in plant defence‐signalling pathways

2006

In plant cells, the calcium ion is a ubiquitous intracellular second messenger involved in numerous signalling pathways. Variations in the cytosolic concentration of Ca2+ ([Ca2+]cyt) couple a large array of signals and responses. Here we concentrate on calcium signalling in plant defence responses, particularly on the generation of the calcium signal and downstream calcium-dependent events participating in the establishment of defence responses with special reference to calcium-binding proteins.

Programmed cell deathPhysiologyGene Expressionchemistry.chemical_elementPlant ScienceBiologyCalciumNitric OxideCytosolPhytoalexinsCalcium-binding proteinCalcium SignalingPhosphorylationPlant DiseasesPlant ProteinsCalcium signalingCell DeathPlant ExtractsTerpenesCalcium-Binding ProteinsPlantsPlant cellElicitorCytosolchemistryBiochemistryCalciumMitogen-Activated Protein KinasesSignal transductionReactive Oxygen SpeciesSesquiterpenesNew Phytologist
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Clusterin gene expression in apoptotic MDCK cells is dependent on the apoptosis-inducing stimulus

1995

Abstract Clusterin (Apolipoprotein J, complement lysis inhibitor) is a widely expressed multifunctional glycoprotein. The expression of clusterin mRNA has been reported to be elevated in a broad spectrum of apoptotic or degenerative tissues. More recently, it was shown that within these tissues clusterin is expressed in the surviving rather than in the dying cells, and that clusterin gene expression is actually down-regulated in the apoptotic cells. We have studied the expression of the clusterin gene in apoptotic MDCK cells. Cell death was initiated by three different stimuli: application of the steroid hormone antagonist RU 486, activation of protein kinase C by the application of the pho…

Programmed cell deathSteroid hormoneApolipoprotein Bmedicine.medical_treatmentCellApoptosisCell LineHormone AntagonistsProtein kinase CmedicineAnimalsRNA MessengerMolecular BiologyProtein kinase CGlycoproteinsRU 486Messenger RNAbiologyClusterinCell BiologyMolecular biologyeye diseasesMifepristoneSteroid hormoneCholesterolmedicine.anatomical_structureClusterinGene Expression RegulationApoptosisCarcinogensbiology.proteinTetradecanoylphorbol Acetatesense organsMolecular ChaperonesBiochimica et Biophysica Acta (BBA) - Molecular Cell Research
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MYC and EGR1 synergize to trigger tumor cell death by controlling NOXA and BIM transcription upon treatment with the proteasome inhibitor bortezomib

2014

The c-MYC (MYC afterward) oncogene is well known for driving numerous oncogenic programs. However, MYC can also induce apoptosis and this function of MYC warrants further clarification. We report here that a clinically relevant proteasome inhibitor significantly increases MYC protein levels and that endogenous MYC is necessary for the induction of apoptosis. This kind of MYC-induced cell death is mediated by enhanced expression of the pro-apoptotic BCL2 family members NOXA and BIM. Quantitative promoter-scanning chromatin immunoprecipitations (qChIP) further revealed binding of MYC to the promoters of NOXA and BIM upon proteasome inhibition, correlating with increased transcription. Both pr…

Programmed cell deathTranscription GeneticEGR1ApoptosisBiologyBortezomibProto-Oncogene Proteins c-mycMicehemic and lymphatic diseasesCell Line TumorProto-Oncogene ProteinsGeneticsmedicineAnimalsPromoter Regions GeneticTranscription factorCells CulturedEarly Growth Response Protein 1Zinc finger transcription factorBinding SitesOncogeneBcl-2-Like Protein 11Genes p16Gene regulation Chromatin and EpigeneticsMembrane ProteinsPromoterGenes p53Boronic AcidsChromatinddc:Gene Expression Regulation NeoplasticProto-Oncogene Proteins c-bcl-2PyrazinesCancer researchProteasome inhibitorApoptosis Regulatory ProteinsProteasome Inhibitorsmedicine.drug
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Evidence for an instructive role of apoptosis during the metamorphosis of Hydractinia echinata (Hydrozoa)

2011

Apoptosis is a highly conserved mechanism of cell deletion that destroys redundant, dysfunctional, damaged, and diseased cells. Furthermore, apoptotic cell death is essential during the development of multicellular organisms. However, there are only a few examples where the occurrence of apoptosis has been shown to be a direct prerequisite for developmental processes. As described previously by our group, the degradation of larval tissue during the first half of the metamorphosis of Hydractinia echinata involves extensive cell death. A large number of cells are removed, and we observed several cellular features of apoptotic cell death in the dying tissue, e.g., nucleosomal DNA fragmentation…

Programmed cell deathmedia_common.quotation_subjectMolecular Sequence DataCellApoptosisContext (language use)Gene Expression Regulation EnzymologicHydractinia echinatamedicineAnimalsAmino Acid SequenceMetamorphosisConserved SequencePhylogenyCaspasemedia_commonbiologyGene Expression ProfilingMetamorphosis Biologicalbiology.organism_classificationCell biologyHydrozoamedicine.anatomical_structureApoptosisCaspasesGene Knockdown Techniquesbiology.proteinDNA fragmentationAnimal Science and ZoologySequence AlignmentZoology
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Berberine inhibits cell growth and mediates caspase-independent cell death in human pancreatic cancer cells.

2010

Pancreatic cancer is one of the most aggressive human malignancies with an increasing incidence worldwide. In addition to the poor survival rates, combinations using gemcitabine as a backbone have failed to show any benefit beyond monotherapy. These facts underscore an urgent need for novel therapeutic options and motivated us to study the effect of berberine on pancreatic cancer cells. Here, we undertook an mRNA-based gene expression profiling study in order to get deeper insight into the molecular targets mediating the growth inhibitory effects of berberine on pancreatic cancer cells compared to normal ones. Twenty-four hours after treatment, berberine showed preferential selectivity towa…

Programmed cell deathmedicine.medical_specialtyBerberineDNA damagePharmaceutical ScienceApoptosisAnalytical Chemistrychemistry.chemical_compoundBerberinePancreatic cancerInternal medicineCell Line TumorDrug DiscoverymedicineHumansRNA MessengerCell ProliferationOligonucleotide Array Sequence AnalysisPharmacologybiologyCell growthTopoisomeraseGene Expression ProfilingOrganic ChemistryCancermedicine.diseaseAntineoplastic Agents PhytogenicCaspase InhibitorsImmunohistochemistryEnzyme ActivationPancreatic NeoplasmsEndocrinologyComplementary and alternative medicinechemistryApoptosisCaspasesbiology.proteinCancer researchMolecular MedicineSignal TransductionPlanta medica
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Extracorporeal shock wave-mediated changes in proliferation, differentiation, and gene expression of human osteoblasts.

2008

The goal of this study was to determine whether cell proliferation, differentiation, and gene expression of primary human osteoblasts (hOB) are influenced by shock wave application (SWA).Osteoblast cultures were isolated from cancellous bone fragments and treated with 500 impulses of energy flux densities of 0.06 mJ/mm, 0.18 mJ/mm, 0.36 mJ/mm, and 0.50 mJ/mm. Twenty-four hours and 96 hours after SWA cell proliferation, alkaline phosphatase activity, and mineralization were analyzed. The global gene expression profiling was determined 96 hours after SWA employing Affymetrix HG-U133A microarrays.After 24 hours, hOB showed a dose-dependent increase in cell proliferation from 68.7% (at 0.06 mJ/…

Proliferation differentiationGene ExpressionIn Vitro TechniquesCritical Care and Intensive Care MedicineHigh-Energy Shock WavesBone DensityGene expressionmedicineHumansHigh-Density MicroarrayOligonucleotide Array Sequence AnalysisOsteoblastsCell growthbusiness.industryReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingOsteoblastCell DifferentiationAnatomyExtracorporeal shock waveAlkaline PhosphataseCell biologyGene expression profilingmedicine.anatomical_structureSurgerybusinessCancellous boneCell DivisionThe Journal of trauma
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