Search results for "Apoptosi"

showing 10 items of 1846 documents

Rilpivirine attenuates liver fibrosis through selective STAT1-mediated apoptosis in hepatic stellate cells

2020

ObjectiveLiver fibrosis constitutes a major health problem worldwide due to its rapidly increasing prevalence and the lack of specific and effective treatments. Growing evidence suggests that signalling through cytokine-activated Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathways regulates liver fibrosis and regeneration. Rilpivirine (RPV) is a widely used anti-HIV drug not reported to produce hepatotoxicity. We aimed to describe the potential hepatoprotective effects of RPV in different models of chronic liver injury, focusing on JAK-STAT signalling regulation.DesignThe effects of RPV on hepatic steatosis, inflammation and fibrogenesis were studied in a nut…

Liver CirrhosisSTAT3 Transcription Factor0301 basic medicineApoptosisRisk AssessmentSensitivity and SpecificityMice03 medical and health sciences0302 clinical medicineNon-alcoholic Fatty Liver DiseaseFibrosisHepatic Stellate CellsmedicineAnimalsHumansSTAT1610 Medicine & healthSTAT3Cells CulturedLiver injurybiologybusiness.industryRilpivirineFatty liverGastroenterologymedicine.diseaseLiver regenerationLiver RegenerationDisease Models AnimalSTAT1 Transcription FactorTreatment Outcome030104 developmental biology030220 oncology & carcinogenesisbiology.proteinHepatic stellate cellCancer researchbusinessJanus kinase
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Liver-specific Ldb1 deletion results in enhanced liver cancer development.

2009

Background & Aims LIM-domain-binding (Ldb) proteins have been demonstrated to be essential not only to key embryonic developmental processes but also to carcinogenesis. We have previously demonstrated Ldb1 to be of high biological and developmental relevance, as a targeted deletion of the Ldb1 gene in mice results in an embryonic lethal and pleiotropic phenotype. Methods We have now established a liver-specific Ldb1 knock out to investigate the role of Ldb1 in carcinogenesis, in particular in hepatocellular carcinoma (HCC) development, in vivo . Results These mice demonstrated a significantly enhanced growth of liver cancer by means of tumor size and number, advocating for an essential role…

Liver Stem CellApoptosisMice TransgenicBiologymedicine.disease_causeArticleMiceCyclin D1Liver Neoplasms ExperimentalmedicineAnimalsRNA MessengerRNA NeoplasmOligonucleotide Array Sequence AnalysisMice KnockoutHepatologyOncogeneBase SequenceMicroarray analysis techniquesCancerLIM Domain Proteinsmedicine.diseaseDNA-Binding ProteinsMice Inbred C57BLLiverImmunologyKnockout mouseCancer researchLiver cancerCarcinogenesisJournal of hepatology
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Concanavalin A?induced T-cell?Mediated hepatic injury in mice: The role of tumor necrosis factor*1

1995

Concanavalin A activates T lymphocytes in vitro and causes T-cell-dependent hepatic injury in mice. T lymphocytes were previously identified as effector cells of concanavalin A-induced liver injury. Here we report that hepatic injury is characterized by apoptotic cell death. On concanavalin A challenge, the cytokines tumor necrosis factor-alpha (TNF alpha), interleukin-2, granulocyte macrophage-colony stimulating factor, and interferon-gamma were detectable in the circulation of the mice. Pretreatment of mice with anti-mouse TNF-alpha antiserum protected them from concanavalin A-induced liver injury. Nude mice failed to release TNF-alpha or interleukin-2 after concanavalin A challenge and w…

Liver injuryHepatologybiologymedicine.medical_treatmentT cellmedicine.diseaseMolecular biologyCytokinemedicine.anatomical_structureGranulocyte macrophage colony-stimulating factorConcanavalin AApoptosisImmunologybiology.proteinmedicineInterferon gammaTumor necrosis factor alphamedicine.drugHepatology
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The role of apoptosis versus oncotic necrosis in liver injury: Facts or faith?

2006

A tightly controlled balance between cell division and cell death is a basic feature for the development and maintenance of liver homeostasis. Disturbances of this balance contribute to liver diseases: too much cell death can cause liver injury, too little cell death is a prerequisite for the development of hepatocellular carcinoma. Thus, a stringent control of the equilibrium of life and death in the liver is necessary. During the last decade most research activities in hepatology dealing with liver injury focussed on the evaluation of apoptosis pathways. Therefore, our understanding of the mechanisms of apoptosis has made profound progress. Programmed cell death (PCD) in the liver enables…

Liver injurymedicine.medical_specialtyProgrammed cell deathNecrosisHepatologyLiver DiseasesApoptosisBiologyHepatologymedicine.diseaseBioinformaticsNecrosisFulminant hepatic failureLiverApoptosisInternal medicineHepatocellular carcinomaImmunologyDeath-inducing signaling complexmedicineAnimalsHumansmedicine.symptomJournal of Hepatology
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pp32/PHAPI determines the apoptosis response of non-small-cell lung cancer

2007

During malignant transformation, cancer cells have to evade cell-intrinsic tumor suppressor mechanisms including apoptosis, thus acquiring a phenotype that is relatively resistant to clinically applied anticancer therapies. Molecular characterization of apoptotic signal transduction defects may help to identify prognostic markers and to develop novel therapeutic strategies. To this end we have undertaken functional analyses of drug-induced apoptosis in human non-small cell-lung cancer (NSCLC) cells. We found that primary drug resistance correlated with defects in apoptosome-dependent caspase activation in vitro. While cytochrome c-induced apoptosome formation was maintained, the subsequent …

Lung NeoplasmsTransplantation HeterologousAntineoplastic AgentsApoptosisMice SCIDBiologyMalignant transformationMiceProstate cancerIn vivoCarcinoma Non-Small-Cell LungmedicineAnimalsHumansLung cancerMolecular BiologyIntracellular Signaling Peptides and ProteinsNuclear ProteinsRNA-Binding ProteinsCancerCell Biologymedicine.diseaseCell biologyEnzyme ActivationApoptosisCaspasesCancer cellCancer researchSignal transductionNeoplasm TransplantationCell Death & Differentiation
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Upon oxidative stress, the antiapoptotic Hsp60/procaspase-3 complex persists in mucoepidermoid carcinoma cells.

2008

Hsp60, a mitochondrial chaperonin highly conserved during evolution, has been found elevated in the cytosol of cancer cells, both in vivo and in vitro, but its role in determining apoptosis during oxidative stress (OS) has not yet been fully elucidated. The aim of the present work was to study the effects of OS on Hsp60 levels and its interactions with procaspase- 3 (p-C3) and p53 in tumor cells. NCI-H292 (mucoepidermoid carcinoma) cells were exposed to various concentrations of hydrogen peroxide (H2O2) for 24 hours. Cell viability was determined by Trypan blue and MTT assays. DNA damage was assessed by the Comet assay, and apoptosis was measured by the AnnexinV cytofluorimetric test. Expos…

Lung Neoplasmsanimal structuresHistologyCell SurvivalDNA damageBlotting WesternBiophysicsHsp60;procaspase-3;mucoepidermoid carcinomaGene ExpressionTetrazolium SaltsApoptosisBiologymedicine.disease_causechemistry.chemical_compoundCell Line TumormedicineHumansChaperonin Hsp60 Cpn60 procaspase-3 caspase- 3 DNA damage p53 apoptosis.Viability assaylcsh:QH301-705.5FormazansCaspase 3Settore BIO/16 - Anatomia UmanaChaperonin 60DNAHydrogen PeroxideTrypan BlueCell BiologyImmunohistochemistryMolecular biologyComet assayOxidative Stresslcsh:Biology (General)chemistryApoptosisCancer cellCarcinoma MucoepidermoidHSP60Trypan blueComet AssayTumor Suppressor Protein p53Oxidative stressDNA Damage
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CD38 expression enhances sensitivity of lymphoma T and B cell lines to biochemical and receptor-mediated apoptosis

2006

CD38 has been widely characterised both as an ectoenzyme and as a receptor. In the present paper, we investigated the role of CD38 as possible modulator of apoptosis. CD38-positive (CD38(+)) and negative (CD38(-)) fractions, obtained by sorting CD38(+) cells from lymphoma T (Jurkat) and lymphoma B (Raji) and by transfecting lymphoma LG14 and myeloid leukemia K562 cell lines, were used. Cellular subpopulations were exposed to different triggers (H(2)O(2), UV-B, alpha-TOS and hrTRAIL) and the extent of apoptosis was determined by Annexin V-FITC/PI assay. Our data showed that, in lymphoma cells, propensity to apoptosis was significantly linked to CD38 expression and that, remarkably, such resp…

Lymphoma B-CellCD30Ultraviolet RaysTocopherolsApoptosisCD38BiologyLymphoma T-CellJurkat cellsTNF-Related Apoptosis-Inducing LigandJurkat Cellsimmune system diseasesAnnexinCell Line Tumorhemic and lymphatic diseasesmedicineHumansVitamin EAnnexin A5B cellhemic and immune systemsHydrogen PeroxideCell BiologyGeneral MedicineOligonucleotides AntisenseFlow CytometryADP-ribosyl Cyclase 1Antigens DifferentiationMolecular biologyBCL10medicine.anatomical_structureApoptosisAnnexin A5K562 CellsFluorescein-5-isothiocyanateCell Biology International
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New Potential Therapeutic Approach for the Treatment of B-Cell Malignancies Using Chlorambucil/Hydroxychloroquine-Loaded Anti-CD20 Nanoparticles

2013

Current B-cell disorder treatments take advantage of dose-intensive chemotherapy regimens and immunotherapy via use of monoclonal antibodies. Unfortunately, they may lead to insufficient tumor distribution of therapeutic agents, and often cause adverse effects on patients. In this contribution, we propose a novel therapeutic approach in which relatively high doses of Hydroxychloroquine and Chlorambucil were loaded into biodegradable nanoparticles coated with an anti-CD20 antibody. We demonstrate their ability to effectively target and internalize in tumor B-cells. Moreover, these nanoparticles were able to kill not only p53 mutated/deleted lymphoma cell lines expressing a low amount of CD20…

Lymphomamedicine.medical_treatmentlcsh:MedicineApoptosisnanoparticles; Targeting strategies; LymphomaAggressive lymphomaMice SCIDPharmacologyAntibodies Monoclonal Murine-DerivedMiceDrug Delivery Systems0302 clinical medicineimmune system diseaseshemic and lymphatic diseasesNANOPARTICLESMedicinelcsh:ScienceCD200303 health sciencesMultidisciplinarybiologyNANOPARTICLES; ANTI-CD20; B-CELL MALIGNANCIESnanoparticleANTI-CD20Flow CytometryImmunohistochemistry3. Good healthDrug CombinationsLeukemia030220 oncology & carcinogenesisMonoclonalTargeting strategieFemaleRituximabRituximabHydroxychloroquineResearch Articlemedicine.drugLymphoma B-CellCell Survival03 medical and health sciencesMicroscopy Electron TransmissionAutophagyB-CELL MALIGNANCIESAnimalsTargeting strategies030304 developmental biologyChlorambucilbusiness.industrylcsh:RHydroxychloroquineImmunotherapyAntigens CD20medicine.diseaseDisease Models Animalbiology.proteinChlorambucillcsh:QbusinessPLoS ONE
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New agents and approaches for targeting the RAS/RAF/MEK/ERK and PI3K/AKT/mTOR cell survival pathways.

2012

The Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR cascades are often activated by genetic alterations in upstream signaling molecules such as receptor tyrosine kinases (RTK). Targeting these pathways is often complex and can result in pathway activation depending on the presence of upstream mutations (e.g., Raf inhibitors induce Raf activation in cells with wild type (WT) RAF in the presence of mutant, activated RAS) and rapamycin can induce Akt activation. Targeting with inhibitors directed at two constituents of the same pathway or two different signaling pathways may be a more effective approach. This review will first evaluate potential uses of Raf, MEK, PI3K, Akt and mTOR inhibitors that have…

MAPK/ERK pathway0303 health sciencesCell signalingbiologyChemistryAKTApoptosisGrowth factorRafOncogens: Signaling pathway3. Good healthMalignant transformation03 medical and health sciences0302 clinical medicineApoptosis030220 oncology & carcinogenesisCancer researchbiology.proteinEpidermal growth factor receptorSignal transductionpi3kProtein kinase BRaPI3K/AKT/mTOR pathway030304 developmental biology
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Inhibitory effects of cynaropicrin on human melanoma progression by targeting MAPK, NF-κB, and Nrf-2 signaling pathways in vitro

2021

Malignant melanoma is the deadliest skin cancer, due to its propensity to metastasize. MAPKs and NF-κB pathways are constitutively activated in melanoma and promote cell proliferation, cell invasion, metastasis formation, and resistance to therapeutic regimens. Thus, they represent potential targets for melanoma prevention and treatment. Phytochemicals are gaining considerable attention for the management of melanoma because of their several cellular and molecular targets. A screening of a small library of sesquiterpenes lactones selected cynaropicrin, isolated from the aerial parts of Centaurea drabifolia subsp. detonsa, for its potential anticancer effect against melanoma cells. Treatment…

MAPK/ERK pathwayApoptosisBiologymedicine.disease_causeLactones03 medical and health scienceschemistry.chemical_compound0302 clinical medicineSettore BIO/10 - Biochimicasesquiterpene lactonesmedicinemelanomaHumansoxidative stresschemopreventionTranscription factorCell ProliferationMitogen-Activated Protein Kinase KinasesPharmacology0303 health sciencesoxidative streCell growthMelanoma030302 biochemistry & molecular biologyNF-kappa BNF-κBmedicine.diseaseMAPKCynaropicrinchemistry030220 oncology & carcinogenesiscynaropicrinDisease ProgressionCancer researchSignal transductionCarcinogenesisSesquiterpenesSignal Transduction
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