Search results for "topoisomerase II"

showing 10 items of 25 documents

New insights into the mechanism of action of pyrazolo[1,2-a]benzo[1,2,3,4]tetrazin-3-one derivatives endowed with anticancer potential

2018

Due to the scarce biological profile, the pyrazolo[1,2-a]benzo[1,2,3,4]tetrazine-3-one scaffold (PBT) has been recently explored as promising core for potential anticancer candidates. Several suitably decorated derivatives (PBTs) exhibited antiproliferative activity in the low-micromolar range associated with apoptosis induction and cell cycle arrest on S phase. Herein, we selected the most active derivatives and submitted them to further biological explorations to deepen the mechanism of action. At first, a DNA targeting is approached by means of flow Linear Dichroism experiments so as to evaluate how small planar molecules might interact with DNA, including the interference with the catal…

0301 basic medicineCell cycle checkpointPyrazolo[1TetrazolesBiochemistrychemistry.chemical_compound0302 clinical medicineSalmonAntiproliferative; DNA-interacting; Intercalation; Linear dichroism; Molecular docking; Pyrazolo[12-a]benzo[1234]tetrazin-3-one; Topoisomerase II; Biochemistry; Molecular MedicineDrug DiscoveryDNA-interactingBase PairingADMEbiologyIntercalating AgentsMolecular Docking Simulation030220 oncology & carcinogenesisMolecular Medicinemedicine.symptomtopoisomerase II3StereochemistryIn silico2Antineoplastic Agentslinear dichroism03 medical and health sciencesantiproliferativeintercalationmedicineAnimalsHumansDNA Cleavage2-a]benzo[1Pharmacology4]tetrazin-3-oneBinding SitesTopoisomeraseOrganic ChemistryDNAmolecular dockingSettore CHIM/08 - Chimica FarmaceuticaChemical spaceProtein Structure TertiaryDNA Topoisomerases Type II030104 developmental biologyMechanism of actionchemistryCatalytic cyclebiology.proteinpyrazolo[12-a]benzo[1234]tetrazin-3-oneDNAChemical Biology & Drug Design
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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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Differential in vitro Anti-HIV Activity of Natural Lignans

1990

Abstract Two naturally occurring lignanolides, isolated from the tropical climbing shrub Ipomoea cairica, (-)-arctigen in and (-)-trachelogen in , were found to inhibit strongly replication of human immunodeficiency virus type 1 (HIV-1; strain HTLV-III B) in vitro. At a concentration of 0.5 (μм , (-)-arctigenin and (-)-trachelogenin inhibited the expression of HIV-1 proteins p 17 and p24 by 80 -90 % and 60 -70 % , respectively. The reverse transcriptase activity in the cul­ture fluids was reduced by 80 -90 % when the cells (HTLV-III B/H 9) were cultivated in the presence of 0.5 μм (-)-arctigen in or 1 μм (-)-trachelogenin . At the same concentrations, the formation of syncytia in the HTLV-I…

Antiviral AgentsLigninLignansGeneral Biochemistry Genetics and Molecular BiologyCell LineMiceStructure-Activity RelationshipViral Proteinschemistry.chemical_compoundAnimalsHumansLeukemia L5178Lignanchemistry.chemical_classificationbiologyTopoisomeraseHIVvirus diseasesDNA topoisomerase II activityMolecular biologyReverse transcriptaseIn vitroDNA Topoisomerases Type IIEnzymechemistryViral replicationCell cultureHIV-1biology.proteinCell DivisionPlasmidsZeitschrift für Naturforschung C
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Synthesis and Antitumor Properties of 2,5-Bis(3'-indolyl) thiophenes: Analogues of Marine Alkaloid Nortopsentin

2007

A series of 11 bis-indolylthiophenes of formula I were obtained by cyclization of bis-indole 1,4-diketones using Lawesson''s reagent. Derivs. I (R = OMe, R1 = SO2Ph), I (R = OMe, R1 = Me), I (R = Cl, R1 = Me), and I (R = OMe, R1 = H) were selected to be evaluated in the full panel of about 60 human tumor cell lines derived from nine human cancer cell types and showed antiproliferative activity generally in the micromolar range. The most sensitive cell lines were: CCRF-CEM, MOLT-4, HL60 (TB), and RPMI-8226 of the leukemia subpanel, HT29 and HCC-2998 cell lines of the colon sub-panel, NCI-H522 of the non-small cell lung cancer sub-panel, LOX IMVI of the melanoma sub-panel, and UO-31 of the re…

Cell typeIndolescyclizationHL60StereochemistryClinical BiochemistryPharmaceutical ScienceAntineoplastic AgentsThiophenesBiochemistryChemical synthesisInhibitory Concentration 50chemistry.chemical_compoundAlkaloids5-bis(3'-indolyl)thiophenesCell Line TumorDrug DiscoverymedicineAnimalsHumansantitumor activityMolecular BiologyCell Proliferationbis-indolylthiopheneCell growthNortopsentinMelanomaOrganic ChemistryImidazolesCancerBiological activityDNAmedicine.diseasediketonesTopoisomerase II5-bis(3'-indolyl)thiophenes; antitumor activity; Topoisomerase II; NortopsentinDNA Topoisomerases Type IIchemistryCell cultureMolecular Medicine
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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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The high rate of endoreduplication in the repair deficient CHO mutant EM9 parallels a reduced level of methylated deoxycytidine in DNA

2008

It has been recently proposed that hypomethylation of DNA induced by 5-azacytidine (5-azaC) leads to reduced chromatid decatenation that ends up in endoreduplication, most likely due to a failure in topo II function [S. Mateos, I. Domínguez, N. Pastor, G. Cantero, F. Cortés, The DNA demethylating 5-azaC induces endoreduplication in cultured Chinese hamster cells, Mutat. Res. 578 (2005) 33-42]. The Chinese hamster mutant cell line EM9 has a high spontaneous frequency of endoreduplication as compared to its parental line AA8. In order to see if this is related to the degree of DNA methylation, we have investigated the basal levels of both endpoints in AA8 and EM9, as well as the effect of ext…

DNA ReplicationDNA RepairHealth Toxicology and MutagenesisMutantCHO CellsChromosome segregationamedicine.disease_causeDeoxycytidineChromosomesChinese hamsterHypomethylation of DNAchemistry.chemical_compoundCricetulusCricetinaeGeneticsmedicineAnimalsEndoreduplicationMolecular BiologyMutationbiologyChinese hamster ovary cellEndoreduplicationDNA Methylationbiology.organism_classificationTopoisomerase IIMolecular biologychemistryMutationDNA methylationAzacitidineChromatidDNAMutation Research/Fundamental and Molecular Mechanisms of Mutagenesis
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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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