Search results for "Apoptosis."

showing 10 items of 1794 documents

Preclinical evaluation of antitumor activity of the proteasome inhibitor MLN2238 (ixazomib) in hepatocellular carcinoma cells

2017

AbstractHepatocellular carcinoma (HCC) is one of the common malignancies and is an increasingly important cause of cancer death worldwide. Surgery, chemotherapy, and radiation therapy extend the 5-year survival limit in HCC patients by only 6%. Therefore, there is a need to develop new therapeutic approaches for the treatment of this disease. The orally bioavailable proteasome inhibitor MLN2238 (ixazomib) has been demonstrated to have anticancer activity. In the present study, we investigated the preclinical therapeutic efficacy of MLN2238 in HCC cells through in vitro and in vivo models, and examined its molecular mechanisms of action. MLN2238 inhibited cell viability in human HCC cells He…

Boron Compounds0301 basic medicineCancer ResearchCarcinoma HepatocellularMyeloidCell cycle checkpointImmunologyCellGlycineAntineoplastic AgentsArticleIxazomibAntineoplastic AgentMice03 medical and health sciencesCellular and Molecular Neurosciencechemistry.chemical_compound0302 clinical medicinemedicineAnimalsHumansViability assaylcsh:QH573-671Boron CompoundAnimallcsh:Cytologybusiness.industryLiver NeoplasmsCell Biologydigestive system diseases3. Good health030104 developmental biologymedicine.anatomical_structurechemistryLiver NeoplasmCell cultureApoptosis030220 oncology & carcinogenesisProteasome inhibitorCancer researchbusinessProteasome InhibitorsHumanmedicine.drugCell Death & Disease
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DHEA-Bodipy–a functional fluorescent DHEA analog for live cell imaging

2009

International audience; The androgen dehydroepiandrosterone (DHEA) has been reported to protect neuronal cells against dysfunction and apoptosis. Several signaling pathways involved in these effects have been described but little is known about the intracellular trafficking of DHEA. We describe design, synthesis and characterization of DHEA-Bodipy, a novel fluorescent DHEA analog. DHEA-Bodipy proved to be a functional DHEA derivative: DHEA-Bodipy (i) induced estrogen receptor α-mediated gene activation, (ii) protected PC12 rat pheochromocytoma cells against serum deprivation-induced apoptosis, and (iii) induced stress fibers and focal adhesion contacts in SH-SY5Y human neuroblastoma cells. …

Boron CompoundsDHEA-Bodipyendocrine systemDehydroepiandrosteroneEstrogen receptorApoptosisBiologyPC12 CellsBiochemistryfluorescence microscopyCell membranegenomicNeuroblastoma03 medical and health sciences0302 clinical medicineEndocrinologynon-genomicGenes ReporterLive cell imagingtraffickingmedicinepolycyclic compoundsAnimalsHumansskin and connective tissue diseasesMolecular BiologyFluorescent Dyes030304 developmental biology0303 health sciencesMolecular StructureCell MembraneEstrogen Receptor alphaBiological TransportDehydroepiandrosteroneRats3. Good healthCell biologylive cell imagingmedicine.anatomical_structureMicroscopy FluorescenceApoptosisSignal transductionEstrogen receptor alphahuman activities030217 neurology & neurosurgeryIntracellularhormones hormone substitutes and hormone antagonists
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Caspase-dependent cell death involved in brain damage after acute subdural hematoma in rats

2006

Abstract Traumatic brain injury is associated with acute subdural hematoma (ASDH) that worsens outcome. Although early removal of blood can reduce mortality, patients still die or remain disabled after surgery and additional treatments are needed. The blood mass and extravasated blood induce pathomechanisms such as high intracranial pressure (ICP), ischemia, apoptosis and inflammation which lead to acute as well as delayed cell death. Only little is known about the basis of delayed cell death in this type of injury. Thus, the purpose of the study was to investigate to which extent caspase-dependent intracellular processes are involved in the lesion development after ASDH in rats. A volume o…

Brain InfarctionMalePathologymedicine.medical_specialtyTraumatic brain injuryIschemiaApoptosisBrain damageNeuroprotectionAmino Acid Chloromethyl KetonesBrain IschemiaRats Sprague-DawleyLesionIn Situ Nick-End LabelingmedicineAnimalsHematoma Subdural AcuteEnzyme InhibitorsSubdural spaceMolecular BiologyIntracranial pressurebusiness.industryVascular diseaseGeneral Neurosciencemedicine.diseaseRatsDisease Models AnimalBloodNeuroprotective AgentsTreatment Outcomemedicine.anatomical_structureBrain InjuriesCaspasesAnesthesiaNeurology (clinical)Intracranial Hypertensionmedicine.symptombusinessSignal TransductionDevelopmental BiologyBrain Research
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A Neuroprotective Function for the Hematopoietic Protein Granulocyte-Macrophage Colony Stimulating Factor (GM-CSF)

2007

Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a hematopoietic cytokine responsible for the proliferation, differentiation, and maturation of cells of the myeloid lineage, which was cloned more than 20 years ago. Here we uncovered a novel function of GM-CSF in the central nervous system (CNS). We identified the GM-CSF α-receptor as an upregulated gene in a screen for ischemia-induced genes in the cortex. This receptor is broadly expressed on neurons throughout the brain together with its ligand and induced by ischemic insults. In primary cortical neurons and human neuroblastoma cells, GM-CSF counteracts programmed cell death and induces BCL-2 and BCL-Xl expression in a dose- a…

Brain InfarctionMaleProgrammed cell deathTime FactorsMyeloidmedicine.medical_treatmentDrug Evaluation Preclinicalbcl-X ProteinApoptosisBiologyNeuroprotectionBrain IschemiaPhosphatidylinositol 3-KinasesmedicineAnimalsHumansMyeloid CellsRats Long-EvansRats WistarProtein kinase BCell ProliferationCerebral CortexNeuronsDose-Response Relationship DrugGrowth factorGranulocyte-Macrophage Colony-Stimulating FactorCell DifferentiationNeurodegenerative DiseasesRatsUp-RegulationCell biologyDisease Models AnimalHaematopoiesisNeuroprotective Agentsmedicine.anatomical_structureGranulocyte macrophage colony-stimulating factorNeurologyBlood-Brain BarrierReceptors Granulocyte-Macrophage Colony-Stimulating FactorImmunologyNeurology (clinical)Signal transductionCardiology and Cardiovascular MedicineProto-Oncogene Proteins c-aktSignal Transductionmedicine.drugJournal of Cerebral Blood Flow & Metabolism
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Exposure to cadmium chloride influences astrocyte-elevated gene-1 (AEG-1) expression in MDA-MB231 human breast cancer cells

2011

Abstract It is known that cadmium (Cd) is able to regulate gene expression, drastically affecting the pattern of transcriptional activity and intracellular signalization in normal and pathological human cells. We have already shown that Cd exerts a cytotoxic effect on neoplastic MDA-MB231 cells from the human breast, which is characterized by the onset of a “non-classical” apoptotic kind of death, impairment of mitochondrial activity and drastic changes in gene expression pattern. In the present study, employing a combination of conventional and differential display-PCR techniques, immunocytochemical, ELISA and Western analyses, we extended the knowledge on the transcriptional modulation ex…

Breast NeoplasmsCadmium chlorideBiologyBiochemistrychemistry.chemical_compoundCadmium ChlorideCell Line TumorGene expressionmedicineHumansCytotoxic T cellSettore BIO/06 - Anatomia Comparata E CitologiaDNA PrimersNucleoplasmBase SequenceReverse Transcriptase Polymerase Chain ReactionBreast cancer cell culture cadmium chloride AEG-1 gene expressionMembrane ProteinsRNA-Binding ProteinsGeneral MedicineImmunohistochemistryMolecular biologyGene Expression Regulation Neoplasticmedicine.anatomical_structurechemistryApoptosisCancer cellFemaleCell Adhesion MoleculesIntracellularAstrocyteBiochimie
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Effects of cadmium chloride on some mitochondria-related activity and gene expression of human MDA-MB231 breast tumor cells.

2007

It was reported that cadmium is able to exert a cytotoxic effect on tumor MDA-MB231 cells, which shows signs of "non-classical" apoptosis and is characterized by drastic changes in gene expression pattern. In this study, we have extended our knowledge of metal-breast cancer cell interactions by analyzing some mitochondria-related aspects of the stress response to CdCl(2) at either 5 or 50 microM 24- or 96-h exposure, by cytochemical, conventional PCR and Northern/Western blot techniques. We demonstrated that (i) no modification of the mitochondrial mass was detectable due to CdCl(2) exposure; (ii) the respiration activity appeared to be increased after 96-h exposures, while the production o…

Breast cancer Cadmium MitochondriaAntineoplastic AgentsApoptosisBreast NeoplasmsMitochondrionCadmium chlorideBiochemistryElectron Transport Complex IVMitochondrial Proteinscadmium mitochondria breast tumor cellsInorganic Chemistrychemistry.chemical_compoundCadmium ChlorideWestern blotCell Line TumorGene expressionmedicineHumansCytochrome c oxidaseSettore BIO/06 - Anatomia Comparata E CitologiaHeat-Shock Proteinsbiologymedicine.diagnostic_testChemistryMolecular biologyMitochondriaOxidative StressGene Expression RegulationApoptosisbiology.proteinHSP60Reactive Oxygen SpeciesIntracellular
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Curcumin as a possible lead compound against hormone-independent, multidrug-resistant breast cancer

2009

We examine the possible evidence that the phytochemical curcumin may overcome resistance to hormonal and cytotoxic agents in breast cancer. We present our observations on MCF-7R, a multidrug-resistant (MDR) variant of the MCF-7 breast cancer cell line. In contrast to MCF-7, MCF-7R lacks aromatase and estrogen receptor alpha (ERalpha) and overexpresses the multidrug transporter ABCB1 and the products of different genes implicated in cell proliferation and survival, like c-IAP-1, NAIP, survivin, and COX-2. Nevertheless, in cytotoxicity and cell death induction assays, we found that the antitumor activity of curcumin is substantial both in MCF-7 and in MCF-7R. We elaborated the diketone system…

Breast cancer multidrug resistance hormone-independencecurcumin analoguesCurcuminAnaloguesAntineoplastic AgentsBreast NeoplasmsPharmacologyMultidrug resistanceGeneral Biochemistry Genetics and Molecular Biologychemistry.chemical_compoundBreast cancerBreast cancerHistory and Philosophy of ScienceCell Line TumorSurvivinmedicineHumansAnalogues; Breast cancer; Curcumin; Hormone-independence; Multidrug resistance;Aromataseskin and connective tissue diseasesCytotoxicitybiologyHormone-independenceGene Expression ProfilingGeneral Neurosciencemedicine.diseaseDrug Resistance MultipleMultiple drug resistancechemistryDrug Resistance NeoplasmApoptosisCurcuminbiology.proteinSettore BIO/14 - FarmacologiaEstrogen receptor alpha
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Carbocysteine counteracts the effects of cigarette smoke on cell growth and on the SIRT1/FoxO3 axis in bronchial epithelial cells

2016

Abstract Background Cigarette smoke may accelerate cellular senescence by increasing oxidative stress. Altered proliferation and altered expression of anti-aging factors, including SIRT1 and FoxO3, characterise cellular senescence. The effects of carbocysteine on the SIRT1/FoxO3 axis and on downstream molecular mechanisms in human bronchial epithelial cells exposed to cigarette smoke are largely unknown. Aims Aim of this study was to explore whether carbocysteine modulated SIRT1/FoxO3 axis, and downstream molecular mechanisms associated to cellular senescence, in a bronchial epithelial cell line (16-HBE) exposed to cigarette smoke. Methods 16HBE cells were stimulated with/without cigarette …

Bronchial epithelial cell0301 basic medicineSenescenceAgingPathologymedicine.medical_specialtyApoptosisSettore MED/10 - Malattie Dell'Apparato RespiratorioBiologyBiochemistryCell LineFlow cytometry03 medical and health sciencesSIRT10302 clinical medicineEndocrinologyGeneticSirtuin 1Western blotSmokeTobaccoSurvivinGeneticsmedicineHumansClonogenic assayMolecular BiologyCellular SenescenceCell ProliferationRegulation of gene expressionmedicine.diagnostic_testCell growthCarbocysteineForkhead Box Protein O3Cigarette smokeEpithelial CellsCarbocysteineCell BiologyCell biologyOxidative Stress030104 developmental biology030220 oncology & carcinogenesisFoxO3Experimental Gerontology
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Multiple in vitro and in vivo regulatory effects of budesonide in CD4+ T lymphocyte subpopulations of allergic asthmatics.

2012

Abstract BACKGROUND: Increased activation and increased survival of T lymphocytes characterise bronchial asthma. OBJECTIVES: In this study the effect of budesonide on T cell survival, on inducible co-stimulator T cells (ICOS), on Foxp3 and on IL-10 molecules in T lymphocyte sub-populations was assessed. METHODS: Cell survival (by annexin V binding) and ICOS in total lymphocytes, in CD4+/CD25+ and in CD4+/CD25- and Foxp3 and IL-10 in CD4+/CD25+ and in CD4+/CD25-cells was evaluated, by cytofluorimetric analysis, in mild intermittent asthmatics (n = 19) and in controls (n = 15). Allergen induced T lymphocyte proliferation and the in vivo effects of budesonide in mild persistent asthmatics (n =…

BudesonideCD4-Positive T-LymphocytesMalePulmonologylcsh:Medicineimmune system diseasesT-Lymphocyte SubsetsMolecular Cell Biologylcsh:ScienceBudesonidecigarette smoke airway epithelial cells reactive oxygen species.MultidisciplinaryT CellsAllergy and HypersensitivityClinical Pharmacologyhemic and immune systemsForkhead Transcription Factorsrespiratory systemMiddle AgedFlow CytometryBronchodilator AgentsInterleukin-10Interleukin 10MedicineFemalemedicine.drugResearch ArticleAdultDrugs and DevicesAdolescentCell SurvivalImmune CellsImmunologychemical and pharmacologic phenomenaInducible T-Cell Co-Stimulator ProteinImmunomodulationIn vivomedicineHumansInducible T-Cell Co-Stimulator ProteinBiologyAsthmaCell Proliferationbusiness.industrylcsh:RT lymphocytemedicine.diseaseIn vitroAsthmarespiratory tract diseasesApoptosisImmunologylcsh:QClinical ImmunologybusinessCytometryPloS one
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Fighting mycobacterial infections by antibiotics, phytochemicals and vaccines.

2011

Buruli ulcer is a neglected disease caused by Mycobacterium ulcerans and represents the world's third most common mycobacterial infection. It produces the polyketide toxins, mycolactones A, B, C and D, which induce apoptosis and necrosis. Clinical symptoms are subcutaneous nodules, papules, plaques and ulcerating oedemae, which can enlarge and destroy nerves and blood vessels and even invade bones by lymphatic or haematogenous spread (osteomyelitis). Patients usually do not suffer from pain or systematic inflammation. Surgery is the treatment of choice, although recurrence is common and wide surgical excisions including healthy tissues result in significant morbidity. Antibiotic therapy wit…

Buruli ulcerNecrosismedicine.drug_classImmunologyAntibioticsBacterial ToxinsInflammationApoptosisQuinolonesMicrobiologyNecrosisBacterial ProteinsmedicineVaccines DNAAnimalsHumansBuruli UlcerbiologyMycobacterium ulceransbusiness.industryOsteomyelitisVaccinationNeglected DiseasesChaperonin 60medicine.diseasebiology.organism_classificationRifamycinsAnti-Bacterial AgentsVaccinationInfectious DiseasesLymphatic systemAminoglycosidesMycobacterium ulceransImmunologyBacterial VaccinesMacrolidesmedicine.symptombusinessPhytotherapyMicrobes and infection
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