Search results for "cell cycle"

showing 10 items of 804 documents

Mechanisms of cell death in canine parvovirus-infected cells provide intuitive insights to developing nanotools for medicine

2010

Jonna Nykky, Jenni E Tuusa, Sanna Kirjavainen, Matti Vuento, Leona GilbertNanoscience Center and Department of Biological and Environmental Science, University of Jyväskylä, FinlandAbstract: Viruses have great potential as nanotools in medicine for gene transfer, targeted gene delivery, and oncolytic cancer virotherapy. Here we have studied cell death mechanisms of canine parvovirus (CPV) to increase the knowledge on the CPV life cycle in order to facilitate the development of better parvovirus vectors. Morphological studies of CPV-infected Norden laboratory feline kidney (NLFK) cells and canine fibroma cells (A72) displayed characteristic apoptotic events. Apoptosis was f…

nekroosianimal diseasesvirusesGene ExpressionPharmaceutical ScienceApoptosisViral Nonstructural Proteinsnecrosis0302 clinical medicineInternational Journal of NanomedicineDrug DiscoveryCaspaseOriginal ResearchMembrane Potential MitochondrialOncolytic Virotherapy0303 health sciencesCell DeathbiologynanoparticleCell Cycleapoptosiscanine parvovirusCanine parvovirusGeneral MedicineFlow Cytometry3. Good healthNanomedicineCaspases030220 oncology & carcinogenesisvirotherapyProgrammed cell deathParvovirus CaninenanopartikkeliBiophysicsBioengineeringDNA FragmentationGene deliveryCell LineBiomaterials03 medical and health sciencesDogsMicroscopy Electron TransmissionAnimalsHumansVirotherapyapoptoosi030304 developmental biologyParvovirusOrganic Chemistrybiology.organism_classificationVirologyOncolytic viruskoiran parvovirusviroterapiaMicroscopy FluorescenceApoptosisCatsbiology.proteinDNA DamageHeLa CellsInternational Journal of Nanomedicine
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Cell-cycle control in cell-biomaterial interactions

2000

Current biocompatibility testing involves the demonstration of cell proliferation, which is usually interpreted as a sign of positive biocompatibility when the materials sustain cell proliferation. As the field of biomaterials research is rapidly moving toward tissue-engineered devices and hybrid organs, control of cell function has become a main topic. Cell function, which involves specific differentiation pathways, cannot be separated from cell-cycle control. The study of cell-cycle control is an important extension of routine proliferation assays and has extensive roots in developmental and tumor biology. We studied the expression of the tumour suppressor gene p53 and the proliferation-a…

p53BiocompatibilityBiomedical EngineeringFOCAL ADHESION KINASEHUMAN BONEPROTEINBiologyFlow cytometryBiomaterialsFocal adhesionbiomaterials testing methodsmedicineKI-67BREAST-CANCERmedicine.diagnostic_testCell growthINDUCTIONPROLIFERATIONBiomaterialCell cycleCell biologyAPOPTOSISEndothelial stem cellFibronectinDNA-DAMAGEImmunologybiology.proteinendothelial cellcell cycleGROWTH ARRESTJournal of Biomedical Materials Research
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In Vitro Cytotoxic Effect of Aqueous Extracts from Leaves and Rhizomes of the Seagrass Posidonia oceanica (L.) Delile on HepG2 Liver Cancer Cells: Fo…

2023

Aqueous extracts from Posidonia oceanica’s green and brown (beached) leaves and rhizomes were prepared, submitted to phenolic compound and proteomic analysis, and examined for their potential cytotoxic effect on HepG2 liver cancer cells in culture. The chosen endpoints related to survival and death were cell viability and locomotory behavior, cell-cycle analysis, apoptosis and autophagy, mitochondrial membrane polarization, and cell redox state. Here, we show that 24 h exposure to both green-leaf- and rhizome-derived extracts decreased tumor cell number in a dose–response manner, with a mean half maximal inhibitory concentration (IC50) estimated at 83 and 11.5 μg of dry extract/mL, respecti…

phenolic compoundreactive oxygen specieSettore CHIM/10 - Chimica Degli AlimentiGeneral Immunology and MicrobiologycaspaseSettore BIO/05 - Zoologiaproteomic analysiscell biology; cell cycle; reactive oxygen species; wound healing assay; caspases; mitochondrial transmembrane potential; clonogenic assay; phenolic compounds; proteomic analysisGeneral Biochemistry Genetics and Molecular Biologycell biologymitochondrial transmembrane potentialcell cycleclonogenic assaySettore BIO/06 - Anatomia Comparata E CitologiaGeneral Agricultural and Biological Scienceswound healing assayBiology
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Aplidin® induces JNK-dependent apoptosis in human breast cancer cells via alteration of glutathione homeostasis, Rac1 GTPase activation, and MKP-1 ph…

2006

Aplidin® is an antitumor agent in phase II clinical trials that induces apoptosis through the sustained activation of Jun N-terminal kinase (JNK). We report that Aplidin® alters glutathione homeostasis increasing the ratio of oxidized to reduced forms (GSSG/GSH). Aplidin® generates reactive oxygen species and disrupts the mitochondrial membrane potential. Exogenous GSH inhibits these effects and also JNK activation and cell death. We found two mechanisms by which Aplidin® activates JNK: rapid activation of Rac1 small GTPase and downregulation of MKP-1 phosphatase. Rac1 activation was diminished by GSH and enhanced by L-buthionine (SR)-sulfoximine, which inhibits GSH synthesis. Downregulatio…

rac1 GTP-Binding ProteinProgrammed cell deathSmall interfering RNAGlutathione reductaseDown-RegulationAntineoplastic AgentsApoptosisBreast NeoplasmsCell Cycle ProteinsBiologyPeptides CyclicImmediate-Early ProteinsMembrane Potentialschemistry.chemical_compoundMiceDownregulation and upregulationDepsipeptidesProtein Phosphatase 1Phosphoprotein PhosphatasesAnimalsHomeostasisHumansMolecular Biologychemistry.chemical_classificationReactive oxygen speciesGlutathione PeroxidaseGlutathione DisulfideJNK Mitogen-Activated Protein KinasesProtein phosphatase 1Dual Specificity Phosphatase 1Cell BiologyGlutathioneCell biologyEnzyme ActivationOxidative StressGlutathione ReductasechemistryMitochondrial MembranesGlutathione disulfideCalciumProtein Tyrosine PhosphatasesReactive Oxygen SpeciesCopperHeLa CellsCell Death and Differentiation
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Biological and Proteomic Characterization of the Anti-Cancer Potency of Aqueous Extracts from Cell-Free Coelomic Fluid of Arbacia lixula Sea Urchin i…

2022

Echinoderms are an acknowledged source of bioactive compounds exerting various beneficial effects on human health. Here, we examined the potential in vitro anti-hepatocarcinoma effects of aqueous extracts of the cell-free coelomic fluid obtained from the sea urchin Arbacia lixula using the HepG2 cell line as a model system. This was accomplished by employing a combination of colorimetric, microscopic and flow cytometric assays to determine cell viability, cell cycle distribution, the possible onset of apoptosis, the accumulation rate of acidic vesicular organelles, mitochondrial polarization, cell redox state and cell locomotory ability. The obtained data show that exposed HepG2 cells under…

reactive oxygen specieSettore CHIM/10 - Chimica Degli AlimentiSettore BIO/05 - ZoologiaHepG2 cellOcean Engineeringapoptosisea urchinechinodermmitochondrial transmembrane potentialcell cycleacidic vesicular organelleSettore BIO/06 - Anatomia Comparata E Citologiacoelomic fluidcoelomic fluid; sea urchin; echinoderm; HepG2 cells; apoptosis; cell cycle; acidic vesicular organelles; mitochondrial transmembrane potential; reactive oxygen species; wound healing assaywound healing assayWater Science and TechnologyCivil and Structural EngineeringJournal of Marine Science and Engineering
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Rho GTPases are over-expressed in human tumors.

1999

Small GTPases of the Rho family are involved in the regulation of a variety of cellular processes, such as the organization of the microfilamental network, cell-cell contact and malignant transformation. To address the question of whether Rho proteins are involved in carcinogenesis in man, we compared their expression in tumors from colon, breast and lung with that of the corresponding normal tissue originating from the same patient. As shown by Rho-specific 32P-ADP-ribosylation, as well as Western-blot analysis, the amount of RhoA protein was largely increased in all 3 types of tumors tested. The most dramatic differences in the expression of Rho GTPases were observed in breast tissue. All…

rho GTP-Binding ProteinsCancer ResearchPathologymedicine.medical_specialtyRHOALung NeoplasmsColonBreast NeoplasmsCell Cycle ProteinsGTPaseCDC42medicine.disease_causeMalignant transformationGTP PhosphohydrolasesGTP-Binding ProteinsmedicineHumansrho-Specific Guanine Nucleotide Dissociation InhibitorsBreastcdc42 GTP-Binding ProteinrhoB GTP-Binding ProteinLungGuanine Nucleotide Dissociation InhibitorsMitogen-Activated Protein Kinase 1Adenosine Diphosphate RibosebiologyCancerMembrane Proteinsmedicine.diseaseImmunohistochemistryrac GTP-Binding ProteinsOncologyrhoC GTP-Binding ProteinCalcium-Calmodulin-Dependent Protein KinasesColonic Neoplasmsbiology.proteinCancer researchImmunohistochemistryCarcinogenesisrhoA GTP-Binding ProteinRhoC GTP-Binding ProteinInternational journal of cancer
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Late Activation of Stress-activated Protein Kinases/c-Jun N-terminal Kinases Triggered by Cisplatin-induced DNA Damage in Repair-defective Cells

2011

Although stress-activated protein kinases/c-Jun N-terminal kinases (SAPK/JNK) are rapidly activated by genotoxins, the role of DNA damage in this response is not well defined. Here we show that the SEK1/MKK4-mediated dual phosphorylation of SAPK/JNK (Thr-183/Tyr-185) correlates with the level of cisplatin-DNA adducts at late times (16–24 h) after drug treatment in both human and mouse cells. Transfection of platinated plasmid DNA also caused SAPK/JNK activation. A defect in transcription-coupled nucleotide excision repair resting on a mutation in Cockayne syndrome group B protein promoted the late SAPK/JNK activation following cisplatin exposure. Signaling to SAPK/JNK was accompanied by act…

rho GTP-Binding ProteinsDNA RepairMAP Kinase Kinase 4DNA repairDNA damageDNA damage response; DNA repair; cisplatin-DNA adducts; SAPK/JNKp38 mitogen-activated protein kinasesAntineoplastic AgentsCell Cycle ProteinsAtaxia Telangiectasia Mutated ProteinsProtein Serine-Threonine KinasesDNA and ChromosomesBiologyBiochemistryAtaxia Telangiectasia Mutated ProteinsDNA AdductsMiceRadiation IonizingAnimalsHumansDNA Breaks Double-StrandedMolecular BiologyReplication protein ACells CulturedMice KnockoutKinaseTumor Suppressor ProteinsJNK Mitogen-Activated Protein KinasesCell BiologyMolecular biologyDNA-Binding ProteinsEnzyme Activationc-Jun N-terminal kinasesbiology.proteinCisplatinSignal TransductionNucleotide excision repairJournal of Biological Chemistry
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Abemaciclib: safety and effectiveness of a unique cyclin-dependent kinase inhibitor

2020

Introduction: The discovery and the clinical availability of novel cyclin-dependent kinases 4 and 6 inhibitors have profoundly changed the therapeutic scenario of metastatic hormone receptor-positive breast carcinoma. Among these inhibitors, abemaciclib can induce potent and sustained cell cycle arrest and immune system stimulation. Areas covered: This review summarizes the safety profile and clinical efficacy data on abemaciclib alone or in combination with aromatase inhibitors or fulvestrant in metastatic hormone receptor-positive breast carcinoma. The management of patients treated with abemaciclib is the object of this paper. Expert opinion: As shown in phase 2 and 3 clinical trials on …

safetyAminopyridinesBreast Neoplasms030204 cardiovascular system & hematology03 medical and health scienceschemistry.chemical_compoundabemaciclib breast cancer metastases hormonal receptors safetybreast cancer0302 clinical medicineBreast cancerCyclin-dependent kinaseAntineoplastic Combined Chemotherapy ProtocolsmedicineHumansPharmacology (medical)metastasesskin and connective tissue diseasesFulvestrantProtein Kinase InhibitorsAbemaciclibbiologyAromatase Inhibitorsbusiness.industryKinasehormonal receptorsCyclin-Dependent Kinase 4Cell Cycle CheckpointsCyclin-Dependent Kinase 6General Medicinemedicine.diseaseAbemaciclibchemistry030220 oncology & carcinogenesisQuality of LifeCancer researchbiology.proteinBenzimidazolesFemalesense organsbusinessHormone
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TP53 mutations and S-phase fraction but not DNA-ploidy are independent prognostic indicators in laryngeal squamous cell carcinoma

2005

To prospectively evaluate the prognostic significance of TP53, H-, K-, and N-Ras mutations, DNA-ploidy and S-phase fraction (SPF) in patients affected by locally advanced laryngeal squamous cell carcinoma (LSCC). Eight-one patients (median follow-up was 71 months) who underwent resective surgery for primary operable locally advanced LSCC were analyzed. Tumor DNA was screened for mutational analysis by PCR/SSCP and sequencing. DNA-ploidy and SPF were performed by flow cytometric analyses. Thirty-six patients (44%) had, at least, a mutation in the TP53 gene. Of them, 22% (8/36) had double mutations and 3% (1/36) had triple mutations. In total, 46 TP53 mutations were observed. The majority (41…

squamous cell carcinomasingle strand conformation polymorphismPrognosipolymerase chain reactionDNA Mutational AnalysisEMTREE drug terms: protein p53 EMTREE medical terms: advanced cancerS PhaseDNA Mutational AnalysiHumansprotein p53 advanced cancer; article; cell cycle S phase; DNA content; exon; flow cytometry; follow up; gene; gene mutation; genetic analysis; histopathology; human; human tissue; larynx carcinoma; multivariate analysis; ploidy; polymerase chain reaction; priority journal; prospective study; single strand conformation polymorphism; squamous cell carcinoma; tp53 gene Carcinoma Squamous Cell; DNA Mutational Analysis; DNA Neoplasm; Genes ras; Humans; Laryngeal Neoplasms; Mutation; Ploidies; Polymorphism Single-Stranded Conformational; Prognosis; S Phase; Survival Rate; Tumor Suppressor Protein p53 [EMTREE drug terms]follow uplarynx carcinomatp53 gene MeSH: Carcinoma Squamous Cellexongene mutationhumanmultivariate analysigeneLaryngeal NeoplasmsPolymorphism Single-Stranded ConformationalLaryngeal NeoplasmPloidiesflow cytometryarticleploidyDNA NeoplasmPrognosisGenes rahuman tissueSurvival RateGenes rascell cycle S phasepriority journalDNA contentgenetic analysiMutationCarcinoma Squamous CellhistopathologyTumor Suppressor Protein p53Ploidieprospective study
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Design, synthesis and structure-activity relationship of 2-(3',4',5'-trimethoxybenzoyl)-benzo[b]furan derivatives as a novel class of inhibitors of t…

2009

The biological importance of microtubules in mitosis and cell division makes them an interesting target for the development of anticancer agents. Small molecules such as benzo[b]furans are attractive as inhibitors of tubulin polymerization. Thus, a new class of inhibitors of tubulin polymerization based on the 2-(3′,4′,5′-trimethoxybenzoyl)-benzo[b]furan molecular skeleton, with electron-donating (Me, OMe or OH) or electron-withdrawing (F, Cl and Br) substituents on the benzene ring, was synthesized and evaluated for antiproliferative activity, inhibition of tubulin polymerization and cell cycle effects. Adding a methyl group at the C-3 position resulted in increased activity. The most prom…

structure-activityStereochemistryClinical BiochemistryPharmaceutical ScienceAntineoplastic Agentsmacromolecular substancesBiochemistryChemical synthesisArticleStructure-Activity Relationshipchemistry.chemical_compoundbenzo[b]furansMicrotubuleCell Line TumorFuranDrug DiscoveryHumansStructure–activity relationshipMolecular BiologyBenzofuransCell ProliferationBinding SitesDose-Response Relationship DrugbiologyChemistryTubulin ModulatorsCell growthCell CycleOrganic ChemistrySmall moleculeTubulin Modulatorstubulin polymerizationTubulinDrug Designbiology.proteinMolecular MedicineProtein MultimerizationColchicine
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