Search results for "Cell killing"

showing 10 items of 30 documents

Selectivity analysis of protein kinase CK2 inhibitors DMAT, TBB and resorufin in cisplatin-induced stress responses.

2009

Udgivelsesdato: 2009-Nov Targeting protein kinases as a therapeutic approach to treat various diseases, especially cancer is currently a fast growing business. Although many inhibitors are available, exhibiting remarkable potency, the major challenge is their selectivity. Here we show that the protein kinase CK2 inhibitors DMAT, TBB and resorufin differ in their selectivity against PI3K family members, since PI3K and DNA-PK are subject to inhibition by DMAT and TBB, however, not by resorufin. TBB and DMAT treatment together with cisplatin lead to an inhibition of cisplatin-induced stress signaling (as detected by phosphorylation of JNK and H2AX). In the case of resorufin no interference wit…

Cancer ResearchKinaseCell SurvivalBlotting WesternAntineoplastic AgentsCell cycleBiologyTriazolesCell killingOncologyBiochemistryApoptosisStress PhysiologicalCell Line TumorOxazinesPhosphorylationHumansBenzimidazolesViability assayCasein kinase 2Signal transductionCisplatinEnzyme InhibitorsCasein Kinase IISignal TransductionInternational journal of oncology
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Ganciclovir-induced apoptosis in HSV-1 thymidine kinase expressing cells: critical role of DNA breaks, Bcl-2 decline and caspase-9 activation.

2002

Although ganciclovir (GCV) is most often used in suicide anticancer gene therapy, the mechanism of GCV-induced cell killing and apoptosis is not fully understood. We analysed the mechanism of apoptosis triggered by GCV using a model system of CHO cells stably transfected with HSV-1 thymidine kinase (HSVtk). GCV-induced apoptosis is due to incorporation of the drug into DNA resulting in replication-dependent formation of DNA double-strand breaks and, at later stages, S and G2/M arrest. GCV-provoked DNA instability was likely to be responsible for the observed initial decline in Bcl-2 level and caspase-9/-3 activation. Further decline in the Bcl-2 level was due to cleavage of the protein by c…

Cancer ResearchTime FactorsvirusesPoly ADP ribose polymeraseApoptosisCytochrome c GroupCHO CellsHerpesvirus 1 HumanTransfectionThymidine KinaseCricetinaeGeneticsAnimalsfas ReceptorMolecular BiologyGanciclovirbiologyReverse Transcriptase Polymerase Chain ReactionCytochrome cCell CycleTransfectionSuicide geneFas receptorMolecular biologyCaspase 9Enzyme ActivationGene Expression Regulation NeoplasticCell killingProto-Oncogene Proteins c-bcl-2ApoptosisThymidine kinaseCaspasesbiology.proteinPoly(ADP-ribose) PolymerasesDNA DamageOncogene
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Drivers of topoisomerase II poisoning mimic and complement cytotoxicity in AML cells

2019

Recently approved cancer drugs remain out-of-reach to most patients due to prohibitive costs and only few produce clinically meaningful benefits. An untapped alternative is to enhance the efficacy and safety of existing cancer drugs. We hypothesized that the response to topoisomerase II poisons, a very successful group of cancer drugs, can be improved by considering treatment-associated transcript levels. To this end, we analyzed transcriptomes from Acute Myeloid Leukemia (AML) cell lines treated with the topoisomerase II poison etoposide. Using complementary criteria of co-regulation within networks and of essentiality for cell survival, we identified and functionally confirmed 11 druggabl…

biologyCombination therapybusiness.industryTopoisomeraseMyeloid leukemiatopoisomerase II poisonscombination therapyCell killingOncologygene expressioncancer essentialitybiology.proteinmedicineCancer researchDNA damageCytotoxic T cellCytotoxicitybusinessEtoposidePI3K/AKT/mTOR pathwayResearch Papermedicine.drugOncotarget
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Loss of ATM sensitizes against O6-methylguanine triggered apoptosis, SCEs and chromosomal aberrations.

2003

A critical pre-cytotoxic and -apoptotic DNA lesion induced by methylating carcinogens and chemotherapeutic drugs is O6-methylguanine (O6MeG). The mechanism by which O6MeG causes cell death via apoptosis is only partially understood. The current model ascribes a role to DNA replication and mismatch repair, which converts O6MeG into a critical distal lesion (presumably a DNA double-strand break) that is finally responsible for genotoxicity and apoptosis. Here we analysed whether the PI3-like kinase ATM is involved in this process. ATM is a major player in recognizing and signaling DNA breaks, but most reports are limited to ionizing radiation. Comparing mouse ATM knockout fibroblasts (ATM-/-)…

Programmed cell deathGuanineDNA damageApoptosisCell Cycle ProteinsAtaxia Telangiectasia Mutated ProteinsBiologyProtein Serine-Threonine Kinasesmedicine.disease_causeBiochemistryMicemedicineCytotoxic T cellAnimalsMolecular BiologyChromosome AberrationsMice KnockoutTumor Suppressor ProteinsCell BiologyTransfectionMolecular biologyDNA-Binding ProteinsCell killingApoptosisDNA mismatch repairSister Chromatid ExchangeGenotoxicityDNA repair
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Apoptosis induced by MNNG in human TK6 lymphoblastoid cells is p53 and Fas/CD95/Apo-1 related.

2003

Agents inducing O(6)-methylguanine (O(6)MeG) in DNA, such as N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), are not only highly mutagenic and carcinogenic but also cytotoxic because of the induction of apoptosis. In CHO fibroblasts, apoptosis triggered by O(6)MeG requires cell proliferation and MutSalpha-dependent mismatch repair and is related to the induction of DNA double-strand breaks (DSBs). Furthermore, it is mediated by Bcl-2 degradation and does not require p53 for which the cells were mutated [Cancer Res. 60 (2000) 5815]. Here we studied cytotoxicity and apoptosis induced by MNNG in a pair of human lymphoblastoid cells expressing wild-type p53 (TK6) and mutant p53 (WTK1) and show tha…

MethylnitronitrosoguanidineCell SurvivalHealth Toxicology and MutagenesisApoptosisCHO CellsBiologyCell LineBcl-2-associated X proteinCricetinaeProto-Oncogene ProteinsGeneticsCytotoxic T cellAnimalsHumansfas Receptorbcl-2-Associated X ProteinMitogen-Activated Protein Kinase 1Cell growthLymphoblastFas receptorMolecular biologyKineticsCell killingProto-Oncogene Proteins c-bcl-2Cell cultureApoptosisbiology.proteinTumor Suppressor Protein p53DNA DamageMutation research
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Physiological Effects of Hyperthermia

1987

Hyperthermia as a modality for the treatment of malignant tumors, either alone or in combination with radiation or anticancer drugs, is rapidly becoming a clinical reality. Three different mechanisms of action have provided the rationale for considering the use of hyperthermia as an antitumor agent. At moderate hyperthermia (T=40˚ -42.5˚ C), heat can increase cell killing in a synergistic way following exposure of a tumor to ionizing radiation. This radiosensitization is probably based on, among other things, the inhibited repair of radiation-induced DNA lesions. Elevated tissue temperatures at 40˚ -42.5˚ C also sensitize tumor cells to certain chemotherapeutic drugs, particularly to alkyla…

HyperthermiaAntitumor activitybusiness.industryContext (language use)medicine.diseaseBleomycinIonizing radiationchemistry.chemical_compoundCell killingchemistryChemosensitizationmedicineCancer researchChemotherapeutic drugsbusiness
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Biodiversity and oenological attitude of Saccharomyces cerevisiae strains isolated in the Montalcino district: biodiversity of S. cerevisiae strains …

2020

ABSTRACT The biodiversity of Saccharomyces cerevisiae was studied in the Montalcino area (Italy). Two wineries were involved in the study, which compared the genotypic and oenological characteristics of the S. cerevisiae strains isolated in spontaneous fermentations. After isolation yeasts were identified by 26S rRNA gene sequence analysis, and S. cerevisiae strains were characterized through interdelta sequence analysis (ISA). Oenological tests were performed in synthetic grape must by varying the magnitude of the main wine-imiting factors. The evolution of alcoholic fermentation was monitored by measuring sugar consumption and flow cytometry. The results revealed the prevalence of S. cere…

PopulationSaccharomyces cerevisiaeWineSaccharomyces cerevisiaeBiologyEthanol fermentationMicrobiologySpecies SpecificityGeneticsFlow cytometryMontalcinoFood scienceeducationMolecular BiologyWineeducation.field_of_studywine biodiversity alcoholic fermentation flow cytometry wild yeast MontalcinoWine biodiversityBiodiversitybiology.organism_classificationWild yeastWineryYeastCell killingItalySettore AGR/16 - MICROBIOLOGIA AGRARIAFermentationAlcoholic fermentationFEMS microbiology letters
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Switchable Bactericidal Effects from Novel Silica-Coated Silver Nanoparticles Mediated by Light Irradiation

2011

Here we report on the triggering of antibacterial activity by a new type of silver nanoparticle coated with porous silica, Ag@silica, irradiated at their surface plasmon resonant frequency. The nanoparticles are able to bind readily to the surface of bacterial cells, although this does not affect bacterial growth since the silica shell largely attenuates the intrinsic toxicity of silver. However, upon simultaneous exposure to light corresponding to the absorption band of the nanoparticles, bacterial death is enhanced selectively on the irradiated zone. Because of the low power density used for the treatments, we discard thermal effects as the cause of cell killing. Instead, we propose that …

SilverSurface PropertiesUltraviolet RaysMetal NanoparticlesNanoparticleMineralogyMicrobial Sensitivity TestsBacterial growthSilver nanoparticleStructure-Activity RelationshipEscherichia coliElectrochemistryGeneral Materials ScienceIrradiationSpectroscopyAntibacterial agentDose-Response Relationship DrugChemistrySurface plasmonSurfaces and InterfacesSilicon DioxideCondensed Matter PhysicsAnti-Bacterial AgentsCell killingAbsorption bandBiophysicsLangmuir
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Porphyrin-bile acid conjugates: from saccharide recognition in the solution to the selective cancer cell fluorescence detection.

2008

This paper describes the preparation and use of conjugates of porphyrins and bile acids as ligands to bind to tumor expressed saccharides. Bile acid-porphyrin conjugates were tested for recognition of saccharides that are typically present on malignant tumor cells. Fluorescence microscopy, in vitro PDT cell killing, and PDT of subcutaneous 4T1 mouse tumors is reported. High selectivity for saccharide cancer markers and cancer cells was observed. This in vivo and in vitro study demonstrated high potential use for these compounds in targeted photodynamic therapy.

GlycosylationPorphyrinsmedicine.drug_classmedicine.medical_treatmentCarbohydratesPhotodynamic therapyApoptosisDNA FragmentationLigandsBiochemistrySensitivity and SpecificityCell LineBile Acids and Saltschemistry.chemical_compoundMiceStructure-Activity RelationshipIn vivoNeoplasmsmedicineFluorescence microscopeBiomarkers TumorAnimalsHumansPhysical and Theoretical ChemistryCell Line TransformedCell ProliferationMice Inbred BALB CBinding SitesBile acidDose-Response Relationship DrugMolecular StructureChemistryOrganic ChemistryCancer3T3 Cellsmedicine.diseasePorphyrinSolutionsCell killingBiochemistryMicroscopy FluorescencePhotochemotherapyCancer cellDrug Screening Assays AntitumorHeLa CellsOrganicbiomolecular chemistry
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The potential of acetaminophen as a prodrug in gene-directed enzyme prodrug therapy.

2000

Acetaminophen is oxidized by human CYP1A2 to the cytotoxic metabolite N-acetylbenzoquinoneimine (NABQI). Incubation of cells transfected with human CYP1A2 (H1A2 MZ cells) with 4-20 mM acetaminophen for 6 hours at 37 degrees C caused extensive cytotoxicity (cell viability10%). In contrast, nontransfected V79 MZ cells were unaffected (viability95%). By mixing H1A2 MZ cells with V79 MZ cells in various proportions and incubating with 4 mM acetaminophen, it was shown that the NABQI released from H1A2 MZ cells also caused cytotoxicity of bystander cells. Thus, in a mixture containing 5% H1A2 MZ cells, exposure to 4 mM acetaminophen for 6 hours resulted in complete cell killing by 24 hours. A sim…

Cancer ResearchCell SurvivalPharmacologyTransfectionCatalysisCell LineCricetulusCytochrome P-450 CYP1A2CricetinaemedicineTumor Cells CulturedCytotoxic T cellAnimalsHumansProdrugsViability assayCytotoxicityMolecular BiologyAcetaminophenChemistryCYP1A2TransfectionGenetic TherapyProdrugAcetaminophenCell killingMolecular Medicinemedicine.drugCancer gene therapy
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