Search results for "Topoisomerase II Inhibitor"

showing 10 items of 14 documents

Resistance of p53 knockout cells to doxorubicin is related to reduced formation of DNA strand breaks rather than impaired apoptotic signaling

2003

The anthracycline doxorubicin (adriamycin) is an important chemotherapeutic agent used in the treatment of solid epithelial and mesenchymal tumors as well as leukemias. A variety of mechanisms has been proposed to be involved in doxorubicin-induced cytotoxicity such as DNA intercalation, oxidative stress, DNA strand breakage by inhibition of topoisomerase II, activation of death receptors, and altered p53 expression. Concerning doxorubicin resistance and p53 status data reported are contradictory. Here, we show that mouse fibroblasts deficient in p53 (p53(-/-)) are more resistant to doxorubicin than p53 wild-type (p53 wt) cells. This is in contrast to other genotoxic agents (UV-light, alkyl…

AnthracyclineApoptosisIn Vitro TechniquesBiochemistryCell LineMicemedicineAnimalsTopoisomerase II InhibitorsDoxorubicinMolecular BiologyEtoposideMice KnockoutbiologyTopoisomeraseCell BiologyFas receptorMolecular biologyDoxorubicinDrug Resistance NeoplasmCell cultureApoptosisCancer researchbiology.proteinTumor Suppressor Protein p53Topoisomerase-II InhibitorDNA DamageSignal Transductionmedicine.drugDNA Repair
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Influence of DNA damage and repair upon the risk of treatment related leukemia

2008

Therapy-related myelodysplasia and acute myeloid leukemia (t-MDS/AML) are malignancies occurring after exposure to chemotherapy and/or radiotherapy. Several studies have addressed cumulative dose, dose intensity and exposure to specific agents of preceding cytotoxic therapy in relation to the risk of developing such leukemia. Since only a small percentage of patients exposed to cytotoxic therapy develop t-MDS/AML, it has been suggested that some genetic predisposition may be involved, specifically associated to polymorphisms in certain genes involved in chemotherapy/radiotherapy response - fundamentally genes intervening in drug detoxification and DNA synthesis and repair. A review is made …

Antimetabolites AntineoplasticCancer ResearchDNA RepairDNA repairDNA damagemedicine.medical_treatmentAntineoplastic AgentsBiologyhemic and lymphatic diseasesmedicineGenetic predispositionHumansTopoisomerase II InhibitorsGenetic Predisposition to DiseaseAntineoplastic Agents AlkylatingChemotherapyPolymorphism GeneticDrug detoxificationMyeloid leukemiaNeoplasms Second PrimaryHematologymedicine.diseaseRadiation therapyLeukemiaOncologyImmunologyCancer researchDNA DamageLeukemia & Lymphoma
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Lovastatin protects human endothelial cells from the genotoxic and cytotoxic effects of the anticancer drugs doxorubicin and etoposide

2006

Background and purpose: 3-Hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins) are frequently used lipid-lowering drugs. Moreover, they exert pleiotropic effects on cellular stress responses and death. Here, we analysed whether lovastatin affects the sensitivity of primary human endothelial cells (HUVEC) to the anticancer drug doxorubicin. Experimental approach: We investigated whether pretreatment of HUVEC with low dose of lovastatin influences the cellular sensitivity to doxorubicin. To this end, cell viability, proliferation and apoptosis as well as DNA damage-triggered stress response were analysed. Key results: Lovastatin reduced the cytotoxic potency of doxorub…

DNA ReplicationCell SurvivalDNA damageApoptosisBiologyPharmacologypolycyclic compoundsmedicineHumansTopoisomerase II InhibitorsDoxorubicinLovastatinEtoposideEtoposideFluorescent DyesPharmacologyAntibiotics AntineoplasticReverse Transcriptase Polymerase Chain ReactionTopoisomeraseCell CycleEndothelial Cellsnutritional and metabolic diseasesAntimutagenic AgentsFibroblastsCell cycleResearch PapersAntineoplastic Agents PhytogenicDoxorubicinDrug Resistance NeoplasmHMG-CoA reductasebiology.proteinlipids (amino acids peptides and proteins)LovastatinHydroxymethylglutaryl-CoA Reductase InhibitorsTopoisomerase-II InhibitorReactive Oxygen SpeciesFluorescein-5-isothiocyanateDNA Damagemedicine.drugBritish Journal of Pharmacology
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Identification of Gip as a novel phage‐encoded gyrase inhibitor protein of Corynebacterium glutamicum

2021

By targeting key regulatory hubs of their host, bacteriophages represent a powerful source for the identification of novel antimicrobial proteins. Here, a screening of small cytoplasmic proteins encoded by the CGP3 prophage of Corynebacterium glutamicum resulted in the identification of the gyrase-inhibiting protein Cg1978, termed Gip. Pull-down assays and surface plasmon resonance revealed a direct interaction of Gip with the gyrase subunit A (GyrA). The inhibitory activity of Gip was shown to be specific to the DNA gyrase of its bacterial host C. glutamicum. Overproduction of Gip in C. glutamicum resulted in a severe growth defect as well as an induction of the SOS response. Furthermore, …

DNA Replicationendocrine systemProtein subunitProphagesBiologyMicrobiologyDNA gyraseCorynebacterium glutamicum03 medical and health scienceschemistry.chemical_compoundViral Proteinsddc:570Topoisomerase II InhibitorsSOS responseMolecular BiologyProphage030304 developmental biology0303 health sciences030306 microbiologyDNA replicationAnti-Bacterial AgentsHigh-Throughput Screening AssaysCorynebacterium glutamicumchemistryBiochemistrybacteriaTopoisomerase-II InhibitorDNAhormones hormone substitutes and hormone antagonistsMolecular Microbiology
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Cisplatin-induced endoreduplication in CHO cells: DNA damage and inhibition of topoisomerase II.

2006

It has been proposed that polyploid cells that arise during a variety of pathological conditions and as a result of exposure to genotoxicants, typically in the liver, become aneuploid through genetic instability. Aneuploidy contributes to, or even drives, tumour development. We have assessed the capacity of the drug cisplatin, one of the most commonly used compounds for the treatment of malignancies, to induce endoreduplication, a particular type of polyploidy, in cultured Chinese hamster AA8 cells. Taking into account that any interference with DNA topoisomerase II (topo II) function leads to endoreduplication, we have found that treatment of the cells with this platinum compound results i…

DNA damageHealth Toxicology and MutagenesisAntineoplastic AgentsCHO CellsPolyploidychemistry.chemical_compoundCricetinaeGeneticsmedicineEndoreduplicationAnimalsHumansTopoisomerase II InhibitorsEnzyme InhibitorsMolecular BiologyCisplatinbiologySettore BIO/16 - Anatomia UmanaTopoisomeraseChinese hamster ovary cellNeoplasms Second PrimaryCell cycleAneugensAneuploidyMolecular biologychemistryTopoisomerase II cisplatinbiology.proteinCancer researchTopoisomerase-II InhibitorCisplatinDNAmedicine.drugDNA Damage
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The DNA topoisomerase II catalytic inhibitor merbarone is genotoxic and induces endoreduplication

2012

Abstract In the last years a number of reports have shown that the so-called topoisomerase II (topo II) catalytic inhibitors are able to induce DNA and chromosome damage, an unexpected result taking into account that they do not stabilize topo II-DNA cleavable complexes, a feature of topo II poisons such as etoposide and amsacrine. Merbarone inhibits the catalytic activity of topo II by blocking DNA cleavage by the enzyme. While it was first reported that merbarone does not induce genotoxic effects in mammalian cells, this has been challenged by reports showing that the topo II inhibitor induces efficiently chromosome and DNA damage, and the question as to a possible behavior as a topo II p…

DNA damageHealth Toxicology and MutagenesisTopoisomerase II; Catalytic inhibitor; Merbarone; DNA damage; Clastogens; EndoreduplicationCatalytic inhibitorCell Linechemistry.chemical_compoundCricetulusCricetinaeGeneticsmedicineEndoreduplicationAnimalsTopoisomerase II InhibitorsClastogenMolecular BiologyAmsacrineCell ProliferationbiologyDNA synthesisCell growthTopoisomeraseMerbaroneCell cycleEndoreduplicationThiobarbituratesMolecular biologyTopoisomerase IIchemistrybiology.proteinDNAmedicine.drugDNA Damage
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Endoreduplication induced in cultured Chinese hamster cells by different anti-topoisomerase II chemicals. Evidence for the essential contribution of …

2004

With the ultimate purpose of testing the hypothesis that, as shown in yeast mutants, any malfunction of DNA topoisomerase II might result in aberrant mitosis due to defective chromosome segregation, we have chosen three chemicals of different nature, recently reported to catalytically inhibit the enzyme. The endpoint selected to assess any negative effect on the ability of topoisomerase II to properly carry out decatenation of fully replicated chromosomes in the G2/M phase of the cell cycle was the presence of metaphases showing diplochromosomes as a result of endoreduplication, i.e. two successive rounds of DNA replication without intervening mitosis. The anti-topoisomerase drugs selected …

Enzyme Inhibitors/pharmacologyCell CycleChromosomeCatalysisChromosomesCatalysiCell LineCricetulusDNA Topoisomerases Type IICricetinaeAnimalsTopoisomerase II InhibitorsDNA Topoisomerases Type II/metabolismEnzyme InhibitorsCell Cycle/geneticCricetulu
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Topoisomerase II inhibition and high yield of endoreduplication induced by the flavonoids luteolin and quercetin

2006

Luteolin and quercetin are widely distributed plant flavonoids that possess a variety of chemical and biological activities, including free-radical scavenging and antioxidant activity. Recently, both flavonoids have been reported to inhibit DNA topoisomerases I and II (topo I and topo II), a property that, together with their ability to induce DNA and chromosome damage, has made them candidate anticancer compounds. In the present study, we confirmed that both compounds are topo II inhibitors by conducting a comparative study of their effect on topo II activity from Chinese hamster ovary AA8 cells. Because interference with the function of topo II to resolve DNA entanglement at the end of re…

Health Toxicology and MutagenesisFlavonoidAntineoplastic AgentsToxicologyTopoisomerase II InhibitorModels BiologicalPolyploidychemistry.chemical_compoundChromosome SegregationCricetinaeGeneticsTopoisomerase II InhibitorsAnimalsEndoreduplicationheterocyclic compoundsEnzyme InhibitorsLuteolinCells CulturedGenetics (clinical)Chromosome AberrationsFlavonoidsEnzyme Inhibitors/pharmacologychemistry.chemical_classificationbiologyTopoisomeraseChinese hamster ovary cellAntineoplastic Agents/adverse effectsDNA Topoisomerases Type IIchemistryBiochemistryDNA Damage/drug effectsFlavonoidbiology.proteinQuercetinDNA Topoisomerases Type II/metabolismTopoisomerase-II InhibitorChromosome Segregation/drug effectsQuercetinAntineoplastic Agents/pharmacologyLuteolinDNADNA DamageMutagenesis
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Photochemical electrocyclisation of 3-vinylindoles to pyrido[2,3-a]-, pyrido[4,3-a]- and thieno[2,3-a]-carbazoles: Design, synthesis, DNA binding and…

2009

In the context of the design and synthesis of DNA ligands, some new hetarene annelated carbazoles were synthesized. As lead structure the intercalating tetracyclic systems pyrido[2,3-a]- and pyrido[4,3-a]-carbazoles and in one case a thieno[2,3-a]-carbazole were taken into account. A dialkyl amino amidic chain was introduced to the planar chromophoric system with the intent to generate minor groove binding properties. The cytotoxicity of some compounds was examined by the NCI antitumor screening. Furthermore, biophysical as well as biochemical studies were performed in order to get some information about the DNA-binding properties and inhibition of DNA related functional enzymes of this new…

IndolesCell SurvivalStereochemistryCarbazolesFluorescence spectrometryAntineoplastic AgentsStereoisomerismContext (language use)Nucleic Acid DenaturationChemical synthesisFluorescenceStructure-Activity RelationshipCell Line TumorDrug DiscoveryAnimalsHumansTopoisomerase II InhibitorsTransition TemperatureStructure–activity relationshipBinding siteCell ProliferationPharmacologyBinding SitesbiologyChemistryCircular DichroismTopoisomeraseCell CycleOrganic ChemistryStereoisomerismDNAGeneral MedicinePhotochemical ProcessesDNA Minor Groove BindingCyclizationDrug Designbiology.proteinCattleSpectrophotometry UltravioletTopoisomerase I InhibitorsEuropean Journal of Medicinal Chemistry
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[Apoptosis of human leukemic cells induced by topoisomerase I and II inhibitors].

1996

International audience; Comparison between five human leukemic lines (BV173, HL60, U937, K562, KCL22) suggest that the main determinant of their sensitivity to topoisomerase I (camptothecin) and II (VP-16) inhibitors is their ability to regulate cell cycle progression in response to specific DNA damage, then to die through apoptosis: the more the cells inhibit cell cycle progression, the less sensitive they are. The final pathway of apoptosis induction involves a cytoplasmic signal, active at neutral pH, needing magnesium, sensitive to various protease inhibitors and activated directly by staurosporine. Modulators of intracellular signaling (calcium chelators, calmodulin inhibitors, PKC mod…

Leukemia[SDV]Life Sciences [q-bio]Cell CycleApoptosisCell DifferentiationDNA Neoplasm[SDV.BC]Life Sciences [q-bio]/Cellular BiologyStaurosporine[SDV] Life Sciences [q-bio]AlkaloidsDNA Topoisomerases Type IIDNA Topoisomerases Type ITumor Cells CulturedHumansTopoisomerase II InhibitorsCamptothecinTopoisomerase I Inhibitors[SDV.BC] Life Sciences [q-bio]/Cellular BiologyProtein Kinase CEtoposideSignal Transduction
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