Search results for "topoisomerase"

showing 10 items of 81 documents

Synthesis and biological evaluation of a D-ring-contracted analogue of lamellarin D

2017

A D-ring contracted analogue of the strongly cytotoxic marine pyrrole alkaloid lamellarin D was synthesized and investigated for its antiproliferative action towards a wild type and a multidrug resistant (MDR) cancer cell line. The compound was found to inhibit tumor cell growth at submicromolar concentrations and showed a lower relative resistance in the MDR cell line than the antitumor drug camptothecin to which lamellarin D shows cross resistance and with which lamellarin D shares the same binding site.

Cell SurvivalStereochemistryClinical BiochemistryPharmaceutical ScienceAntineoplastic Agents010402 general chemistryHeterocyclic Compounds 4 or More Rings01 natural sciencesBiochemistrychemistry.chemical_compoundCoumarinsCell Line TumorDrug DiscoverymedicineHumansCytotoxic T cellheterocyclic compoundsBinding siteMolecular BiologyBinding Sites010405 organic chemistryChemistryAlkaloidOrganic ChemistryWild typeIsoquinolinesProtein Structure Tertiary0104 chemical sciencesG2 Phase Cell Cycle CheckpointsMolecular Docking SimulationMultiple drug resistanceDNA Topoisomerases Type IDrug Resistance NeoplasmMutagenesisCell cultureLamellarin DM Phase Cell Cycle CheckpointsMolecular MedicineTopoisomerase I InhibitorsCamptothecinmedicine.drugBioorganic & Medicinal Chemistry
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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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The HMG-CoA reductase inhibitor lovastatin protects cells from the antineoplastic drugs doxorubicin and etoposide

2002

Ras-homologous GTPases are involved in the regulation of genotoxic stress-induced gene expression and cell death. Since they need C-terminal isoprenylation for correct intracellular localization and function, we investigated whether depletion of cells from isopren precursor moieties using the HMG-CoA reductase inhibitor lovastatin affects cellular sensitivity to DNA damaging drugs. Here we show that lovastatin renders cells highly resistant to the tumor-therapeutic compound doxorubicin. Desensitization by lovastatin was reverted by co-treatment with GGPP indicating that inhibition of protein geranylgeranylation is involved in acquired doxorubicin resistance. Lovastatin does not influence ce…

CisplatinStatinbiologymedicine.drug_classTopoisomerasenutritional and metabolic diseasesGeneral MedicinePharmacologyHMG-CoA reductasepolycyclic compoundsGeneticsmedicinebiology.proteinCancer researchDNA fragmentationlipids (amino acids peptides and proteins)DoxorubicinLovastatinEtoposidemedicine.drugInternational Journal of Molecular Medicine
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Luminescent Pt-II and Pt-IV Platinacycles with Anticancer Activity Against Multiplatinum-Resistant Metastatic CRC and CRPC Cell Models

2020

Platinum-based chemotherapy persists to be the only effective therapeutic option against a wide variety of tumours. Nevertheless, the acquisition of platinum resistance is utterly common, ultimately cornering conventional platinum drugs to only palliative in many patients. Thus, encountering alternatives that are both effective and non-cross-resistant is urgent. In this work, we report the synthesis, reduction studies, and luminescent properties of a series of cyclometallated (C,N,N')PtIV compounds derived from amine- imine ligands, and their remarkable efficacy at the high nanomolar range and complete lack of cross57 resistance, as an intrinsic property of the platinacycle, against multipl…

Colorectal cancermedicine.medical_treatment010402 general chemistry01 natural sciencesCatalysisProstate cancermedicineLung cancerCàncerPlatíPlatinumCancerCisplatinChemotherapybiology010405 organic chemistryChemistryPhosphorescenceTopoisomeraseOrganic ChemistryCancerGeneral Chemistrymedicine.disease0104 chemical sciencesCancer cellbiology.proteinCancer researchFosforescènciamedicine.drug
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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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Mechanisms of quinolone resistance in Aeromonas species isolated from humans, water and eels.

2009

Mechanisms of resistance were determined in 33 quinolone-resistant isolates of the species Aeromonas hydrophila, Aeromonas caviae, Aeromonas media, Aeromonas salmonicida, Aeromonas popoffii and Aeromonas veronii, recovered from humans, freshwater and eels. The quinolone resistance-determining regions (QRDRs) of gyrA and parC genes were sequenced in these resistant strains, as well as in 8 quinolone-sensitive Aeromonas used as controls. All quinolone-resistant Aeromonas carried point mutations in the gyrA QRDR at codon 83, respectively giving rise to substitutions Ser(83)-->Ile (32 strains) or Ser(83)-->Val (1 strain). Almost half of these isolates (48%) carried additional point mutations in…

DNA Topoisomerase IVDNA BacterialAeromonas caviaemedicine.drug_classDNA Mutational AnalysisMutation MissenseDrug resistanceMicrobial Sensitivity TestsQuinolonesMicrobiologyMicrobiologyBacterial ProteinsDrug Resistance BacterialmedicineAnimalsHumansPoint MutationMolecular BiologyEelsbiologyGeneral MedicineSequence Analysis DNAbiochemical phenomena metabolism and nutritionQuinolonebiology.organism_classificationAnti-Bacterial AgentsAeromonas hydrophilaAeromonas salmonicidaAeromonasAmino Acid SubstitutionDNA GyraseAeromonas mediaAeromonasGram-Negative Bacterial InfectionsWater MicrobiologyAeromonas veroniiResearch in microbiology
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Spontaneous Quinolone Resistance in the Zoonotic Serovar of Vibrio vulnificus

2009

ABSTRACT This work demonstrates that Vibrio vulnificus biotype 2, serovar E, an eel pathogen able to infect humans, can become resistant to quinolone by specific mutations in gyrA (substitution of isoleucine for serine at position 83) and to some fluoroquinolones by additional mutations in parC (substitution of lysine for serine at position 85). Thus, to avoid the selection of resistant strains that are potentially pathogenic for humans, antibiotics other than quinolones must be used to treat vibriosis on farms.

DNA Topoisomerase IVDNA BacterialSerotypeBiologiamedicine.drug_classMolecular Sequence DataAntibioticsMutation MissenseMicrobiologiaPublic Health MicrobiologyVibrio vulnificusQuinolonesApplied Microbiology and BiotechnologyDNA gyraseMicrobiologyBacterial ProteinsVibrionaceaeDrug Resistance BacterialmedicineAnimalsVibrio vulnificusPathogenEelsEcologybiologySequence Analysis DNAbiology.organism_classificationQuinoloneVirologyAnti-Bacterial AgentsDNA GyrasebacteriaBacteriaFood ScienceBiotechnologyApplied and Environmental 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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