Search results for "CELL SURVIVAL"

showing 10 items of 870 documents

Heme oxygenase-1 inhibits apoptosis in Caco-2 cells via activation of Akt pathway

2005

Heme oxygenase-1 can play a protective role against cellular stress. In colon cancer cells, these effects would be relevant to oncogenesis and resistance to chemotherapy. The aim of the study was to examine the effects of heme oxygenase-1 induction on cell survival in a human colon cancer cell line, Caco-2. Serum deprivation induced apoptosis, reduced Akt and p38 phosphorylation, and increased p21(Cip/WAF1) levels. Heme oxygenase-1 induction by treatment with cobalt protoporphyrin IX resulted in resistance to apoptosis, activation of Akt, reduction in p21(Cip/WAF1) levels and modification of bcl2/bax ratio towards survival. Indomethacin reduced apoptosis but in contrast to heme oxygenase-1,…

Cyclin-Dependent Kinase Inhibitor p21BiliverdinCell SurvivalChemistryBilirubinp38 mitogen-activated protein kinasesProtoporphyrinsApoptosisCell BiologyBiochemistryCulture Media Serum-FreeCell biologyHeme oxygenasechemistry.chemical_compoundApoptosisEnzyme InductionHumansCaco-2 CellsProto-Oncogene Proteins c-aktHemeProtein kinase BHeme Oxygenase-1PI3K/AKT/mTOR pathwayThe International Journal of Biochemistry & Cell Biology
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Observations on the effects of cyclophosphamide, phosphoramide mustard and some activated oxazaphosphorines on murine L1210 leukemia.

1984

The L1210 tumor system was used in vitro and in vivo in comparative studies with activated cyclophosphamide analogs, cyclophosphamide and phosphoramide mustard. All the above compounds gave substantial cell kills (5 logs) of L1210 in vivo at doses that were non-toxic, but slight differences were noted. ASTA Z 7557 had a slight advantage in cure rate over cyclophosphamide when these drugs were given i.v. or i.p. to early tumor (i.p.). However, cyclophosphamide had the advantage in cure rate when drug administration was i.v. to advanced tumor. At equimolar concentrations in vitro ASTA Z 7557 was more cytotoxic than either phosphoramide mustard or acrolein. In vivo, the activated cyclophospham…

CyclophosphamideCell SurvivalPharmacologychemistry.chemical_compoundMiceFibrosisIn vivomedicineAnimalsPharmacology (medical)Clonogenic assayLeukemia L1210CyclophosphamideTumor Stem Cell AssayPharmacologyMice Inbred BALB CDose-Response Relationship Drugbusiness.industryAcroleinTumor Stem Cell Assaymedicine.diseasePhosphoramide MustardIn vitroOncologychemistryMice Inbred DBAPhosphoramide Mustardsbusinessmedicine.drugInvestigational new drugs
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Neuronal Bioenergetics and Acute Mitochondrial Dysfunction: A Clue to Understanding the Central Nervous System Side Effects of Efavirenz

2014

Background. Neurological pathogenesis is associated with mitochondrial dysfunction and differences in neuronal/glial handling of oxygen and glucose. The main side effects attributed to efavirenz involve the CNS, but the underlying mechanisms are unclear. Methods. Human cell lines and rat primary cultures of neurons and astrocytes were treated with clinically relevant efavirenz concentration. Results. Efavirenz alters mitochondrial respiration, enhances reactive oxygen species generation, undermines mitochondrial membrane potential, and reduces adenosine triphosphate (ATP) levels in a concentration-dependent fashion in both neurons and glial cells. However, it activates adenosine monophospha…

CyclopropanesCell SurvivalCell RespirationPharmacologyMitochondrionBiologymedicine.disease_causechemistry.chemical_compoundOxygen ConsumptionHIV-associated neurocognitive disordersSuperoxidesnitric oxideCell Line TumorneurotoxicitymedicineAnimalsHumansImmunology and AllergyGlycolysisRats WistarMembrane Potential MitochondrialNeuronsMembrane potentialDose-Response Relationship DrugNeurotoxicityHIVefavirenzmedicine.diseasecentral nervous systemAdenosineBenzoxazinesMitochondriaRatsmitochondriaInfectious Diseasesmedicine.anatomical_structurechemistrynervous systemAlkynesAstrocytesReverse Transcriptase InhibitorsNeurogliaEnergy MetabolismNeurogliaAdenosine triphosphateOxidative stressmedicine.drug
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Autophagy as a rescue mechanism in efavirenz-induced mitochondrial dysfunction: a lesson from hepatic cells.

2011

Efavirenz (EFV) is the most widely used non-nucleoside reverse transcriptase inhibitor applied in highly active antiretroviral therapy (HAART), the combined pharmacological treatment of the human immunodeficiency virus infection. Its use has been associated with the development of several adverse events including hepatotoxicity. The molecular pathogenesis of this effect is poorly understood but recent reports have highlighted features of mitochondrial dysfunction in hepatic cells exposed to clinically relevant concentrations of EFV. In this study, we investigated the activation of autophagy and, in particular, mitophagy, in human hepatic cells exposed to EFV. We detected the presence of alt…

CyclopropanesEfavirenzCell SurvivalMitochondrionBiologyModels Biologicalchemistry.chemical_compoundMitophagymedicineAutophagyHumansMolecular BiologyReverse-transcriptase inhibitorAutophagyCell BiologyBenzoxazinesMitochondriachemistryApoptosisAlkynesImmunologyCancer researchHepatic stellate cellHepatocytesReverse Transcriptase InhibitorsHomeostasismedicine.drugAutophagy
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Compromising mitochondrial function with the antiretroviral drug efavirenz induces cell survival-promoting autophagy

2011

Hepatotoxicity is a very common side effect associated with the pharmacological treatment of human immunodeficiency virus (HIV) infection and its pathogenesis is poorly understood. Efavirenz (EFV) is the most widely used nonnucleoside reverse transcriptase inhibitor administered for the control of HIV and some of its toxic effects in hepatic cells have been recently shown to display features of mitochondrial dysfunction. Here we studied the activation of autophagy and, in particular, mitophagy, the main mitochondrial turnover mechanism, in human hepatic cells treated with clinically relevant concentrations of this drug. EFV-treated cells had altered mitochondria, characterized by a relative…

CyclopropanesEfavirenzHepatologyAnti-HIV AgentsCell SurvivalMitochondrial TurnoverAutophagyVacuoleMitochondrionBiologyBenzoxazinesMitochondriaCell biologychemistry.chemical_compoundchemistryApoptosisAlkynesMitophagyAutophagyCancer researchHepatic stellate cellHumansChemical and Drug Induced Liver InjuryHeLa CellsHepatology
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Enhanced oxidative stress and increased mitochondrial mass during Efavirenz-induced apoptosis in human hepatic cells

2010

BACKGROUND AND PURPOSE Efavirenz (EFV) is widely used in the treatment of HIV-1 infection. Though highly efficient, there is growing concern about EFV-related side effects, the molecular basis of which remains elusive. EXPERIMENTAL APPROACH In vitro studies were performed to address the effect of clinically relevant concentrations of EFV (10, 25 and 50 mu M) on human hepatic cells. KEY RESULTS Cellular proliferation and viability were reduced in a concentration-dependent manner. Analyses of the cell cycle and several cell death parameters (chromatin condensation, phosphatidylserine exteriorization, mitochondrial proapoptotic protein translocation and caspase activation) revealed that EFV tr…

CyclopropanesMalehepatotoxicityCarcinoma HepatocellularTime FactorsAnti-HIV AgentsCell SurvivalApoptosisMitochondria LiverPhosphatidylserinesAntioxidantsSuperoxidesHumansChromansantiretroviral drugsCell Proliferationreactive oxygen speciesDose-Response Relationship DrugCell CycleLiver NeoplasmsChromatin Assembly and DisassemblyResearch PapersGlutathioneBenzoxazinesmitochondriaOxidative Stressside effectscell deathLiverAlkynesFemaleEfavirenzApoptosis Regulatory ProteinsHeLa Cells
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Biochemical and chemical characterization of Cynara cardunculus L. extract and its potential use as co-adjuvant therapy of chronic myeloid leukemia

2017

Abstract Ethnopharmacological relevance Ancient mediterranean diet was characterized by consuming the spontaneous forms of Cynara cardunculus L. (CCL), commonly called artichoke. Cultivated and/or spontaneous forms of CC studies have demonstrated that methanol extract of CCL flower and/or cynaropicrin showed remarkable anti-proliferative activity in vitro models of leukocyte cancer cell. Aim of the study Chronic myeloid leukemia (CML) is associated with a reciprocal translocation of the long arms of chromosomes 9 and 22 generating the BCR/ABL fusion gene, translated in the p210 BCR/ABL oncoprotein kinase. This chimeric protein is the target of a kinase inhibitor, imatinib, but the developme…

Cynara cardunculus L.Sesquiterpene0301 basic medicineSettore MED/06 - Oncologia MedicaFusion Proteins bcr-ablPharmacologyAntineoplastic AgentLactoneschemistry.chemical_compound0302 clinical medicinehemic and lymphatic diseasesDrug DiscoveryK562 cellABLChemistryChronic myeloid leukemiabreakpoint cluster regionMyeloid leukemiaLactoneCynaropicrinImatinib resistantChemotherapy Adjuvant030220 oncology & carcinogenesisImatinib MesylateChronic myeloid leukemia; Cynara cardunculus L.; Imatinib resistant; K562 cells; P210BCR/ABLoncoprotein; Antineoplastic Agents; Antineoplastic Agents Phytogenic; Cell Survival; Chemotherapy Adjuvant; Cynara; Drug Resistance Neoplasm; Fusion Proteins bcr-abl; Humans; Imatinib Mesylate; K562 Cells; Lactones; Leukemia Myelogenous Chronic BCR-ABL Positive; Plant Extracts; Sesquiterpenes; Pharmacology; Drug Discovery3003 Pharmaceutical ScienceSesquiterpenesHumanmedicine.drugCell SurvivalAntineoplastic AgentsCynaraPlant Extract03 medical and health sciencesLeukemia Myelogenous Chronic BCR-ABL PositivemedicineHumansViability assayneoplasmsPharmacologyPlant ExtractsCell growthDrug Discovery3003 Pharmaceutical ScienceImatinibAntineoplastic Agents PhytogenicP210BCR/ABLoncoprotein030104 developmental biologyDrug Resistance NeoplasmCancer researchK562 CellsK562 cellsJournal of Ethnopharmacology
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T cells engineered to express a T-cell receptor specific for glypican-3 to recognize and kill hepatoma cells in vitro and in mice

2015

Background & Aims Cancer therapies are being developed based on our ability to direct T cells against tumor antigens. Glypican-3 (GPC3) is expressed by 75% of all hepatocellular carcinomas (HCC), but not in healthy liver tissue or other organs. We aimed to generate T cells with GPC3-specific receptors that recognize HCC and used them to eliminate GPC3-expressing xenograft tumors grown from human HCC cells in mice. Methods We used mass spectrometry to obtain a comprehensive peptidome from GPC3-expressing hepatoma cells after immune-affinity purification of human leukocyte antigen (HLA)-A2 and bioinformatics to identify immunodominant peptides. To circumvent GPC3 tolerance resulting from feta…

Cytotoxicity ImmunologicCancer Immunotherapy ; Immune Response ; Liver Cancer ; Tumor-associated AntigensCarcinoma HepatocellularTime FactorsCell SurvivalMice SCIDCD8-Positive T-LymphocytesBiologyLymphocyte ActivationTransfectionImmunotherapy AdoptiveInterferon-gammaInterleukin 21GlypicansHLA-A2 AntigenAnimalsHumansCytotoxic T cellIL-2 receptorAntigen-presenting cellInterleukin 3HepatologyImmunodominant EpitopesZAP70Liver NeoplasmsGastroenterologyDendritic CellsHep G2 CellsNatural killer T cellXenograft Model Antitumor AssaysMolecular biologyCoculture TechniquesGenes T-Cell ReceptorInterleukin 12FemaleGenetic Engineering
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FOXP3 Inhibitory Peptide P60 Increases Efficacy of Cytokine-induced Killer Cells Against Renal and Pancreatic Cancer Cells

2019

Background/aim Cytokine-induced killer (CIK) cells are ex vivo expanded major histocompatibility complex (MHC)-unrestricted cytotoxic cells with promising effects against a variety of cancer types. Regulatory T-cells (T-reg) have been shown to reduce the effectiveness of CIK cells against tumor cells. Peptide P60 has been shown to inhibit the immunosuppressive functions of T-regs. This study aimed at examining the effect of p60 on CIK cells efficacy against renal and pancreatic cancer cells. Materials and methods The effect of P60 on CIK cytotoxicity was examined using flow cytometry, WST-8-based cell viability assay and interferon γ (IFNγ) ELISA. Results P60 treatment resulted in a signifi…

Cytotoxicity ImmunologicCancer ResearchFOXP3Cell SurvivalImmunotherapy.KidneyMajor histocompatibility complexT-Lymphocytes RegulatoryInterferon-gamma03 medical and health sciencesCytokine-Induced Killer Cells0302 clinical medicineCytokine-induced killer (CIK) cellCell Line TumorPancreatic cancermedicineHumansCytotoxic T cellViability assayCytotoxicityPancreasCancerCytokine-induced killer cellbiologyChemistryFOXP3Forkhead Transcription FactorsGeneral Medicinemedicine.diseaseCoculture TechniquesKidney NeoplasmsPancreatic NeoplasmsOncologyCell culture030220 oncology & carcinogenesisAdoptive cell transferCancer researchbiology.proteinCytokinesPeptidesAnticancer Research
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Cytotoxic T cells with reciprocal antigenic peptide presentation function are not generally resistant to mutual lysis

2003

Cytotoxic T cells normally express major histocompatibility complex class I molecules, to which their T cell antigen receptors are restricted. Therefore, a single cytotoxic T cell can not only act as a cytolytic effector cell, but also as an antigen-presenting cell for other cytotoxic T cells of the same or a different clone. In the present paper, we used a murine cytotoxic T cell clone, 10BK.1, recognizing the ovalbumin-derived peptide OVA257-264 in combination with H-2Kb to investigate the consequences of reciprocal antigen presentation by these cytotoxic T cells. These cells proliferate after incubation with the relevant peptide in the absence of added accessory cells, indicating recipro…

Cytotoxicity ImmunologicCell SurvivalOvalbuminImmunologyAntigen presentationDose-Response Relationship ImmunologicBiologyLymphocyte ActivationMiceInterleukin 21AntigenAnimalsImmunology and AllergyCytotoxic T cellAntigen-presenting cellAntigen PresentationLymphokine-activated killer cellAntibodies MonoclonalCell BiologyCytotoxicity Tests ImmunologicFlow CytometryNatural killer T cellMolecular biologyPeptide FragmentsClone CellsCell biologyInterleukin 12Interleukin-2T-Lymphocytes CytotoxicImmunology & Cell Biology
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