Search results for "Cell Cycle"

showing 10 items of 804 documents

In silico characterization of LZTS3, a potential tumor suppressor

2005

Members of the leucine zipper tumor suppressor (LZTS) protein family are thought to play roles in cell growth modulation. The two currently known members were identified by analyzing genomic and chromosomal alterations reported to be either involved or deleted in various types of cancer, suggesting a causative relationship. By means of computational biology, we have now identified a novel member of the LZTS protein family named LZTS3. The corresponding gene was localized to chromosome 20p13 and consisted of three exons. The novel LZTS3 protein demonstrated a high similarity to LAPSER1/LZTS2 and FEZ1/LZTS1, two members of the LZTS family. The conserved FEZ1 domain contains a leucine zipper m…

GeneticsCancer ResearchLeucine zipperOncologyTumor suppressor geneProtein familyIn silicoActivating transcription factorGeneral MedicineBiologyCell cycleFEZ1Transcription factorOncology Reports
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Flow Cytometry and Karyotype Analysis ofD. melanogasterEye Disc Cells

2008

The developing Drosophila eye-antennal disc is a particularly suited system for the genetic and cellular studies of complex biological processes. Methods to analyze Drosophila eye discs by flow cytometry are mainly based on the dissociation of tissues with trypsin. Dissociation operated by trypsin is very effective, though it causes a lot of stress to live cells often compromising the use of treated cells for further analyses. Here, we report a method to produce dissociated eye-disc cells that retain cell-membrane markers and that can be used for flow cytometry and cytological analysis of mitotic chromosomes. The method described is a great complementing tool for the cellular characterizati…

Geneticsbiologymedicine.diagnostic_testKaryotypeEyeFlow Cytometrybiology.organism_classificationTrypsinPhenotypeChromosomesFlow cytometryCell biologyDrosophila melanogasterKaryotypingLarvaInsect SciencemedicineMelanogasterAnimalsDrosophila melanogasterMitosisCell cycle Drosophila Eye-antennal disc Flow cytometry Mitotic chromosomemedicine.drugFly
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Bypass of cell cycle arrest induced by transient DNMT1 post-transcriptional silencing triggers aneuploidy in human cells

2012

Abstract Background Aneuploidy has been acknowledged as a major source of genomic instability in cancer, and it is often considered the result of chromosome segregation errors including those caused by defects in genes controlling the mitotic spindle assembly, centrosome duplication and cell-cycle checkpoints. Aneuploidy and chromosomal instability has been also correlated with epigenetic alteration, however the molecular basis of this correlation is poorly understood. Results To address the functional connection existing between epigenetic changes and aneuploidy, we used RNA-interference to silence the DNMT1 gene, encoding for a highly conserved member of the DNA methyl-transferases. DNMT1…

Genome instabilityCell cycle checkpointDNA damageAneuploidyBiologylcsh:RC254-282BiochemistryChromosome instabilitymedicineCentrosome duplicationEpigeneticsaneuploidylcsh:QH573-671Molecular BiologyGeneticsDNA methylationG1 arrestlcsh:CytologyResearchDNMT1Cell Biologylcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseCell biologySettore BIO/18 - GeneticaDNMT1 Aneuploidy epigenetic p14/ARF siRNADNA methylation
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Regulation of cytokinesis and its clinical significance.

2015

Dysregulation of the cell cycle leads to polyploid cells, which are classified into mononuclear or binuclear polyploid cells depending on the number of nuclei. Polyploidy is common in plants and in animals. Physiologically, polyploidy and binucleation are differentiation markers and also features of the aging process. In fact, although they provide multiple copies of genes required for survival, a negative correlation between growth capacity and polyploidy has been reported, and thus, suppression or reversal of this phenomenon may be a growth advantage. On the other hand, unscheduled polyploidization may cause genomic instability that might lead to neoplastic aneuploidy. The aim of this rev…

Genome instabilityClinical BiochemistryBiologymedicine.disease_causeGeneral Biochemistry Genetics and Molecular BiologyMicemedicineAnimalsHumansPI3K/AKT/mTOR pathwayCells CulturedCytokinesisLiver injuryGeneticsMice KnockoutBiochemistry (medical)Cell CycleLiver NeoplasmsCell cyclemedicine.diseaseLiver regenerationCell biologyLiver Regenerationmedicine.anatomical_structureHepatocyteHepatocytesCarcinogenesisCytokinesisCritical reviews in clinical laboratory sciences
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MAD2 depletion triggers premature cellular senescence in human primary fibroblasts by activating a P53 pathway preventing aneuploid cells propagation.

2012

The spindle assembly checkpoint (SAC) is a cellular surveillance mechanism that ensures faithful chromosome segregation during mitosis and its failure can result in aneuploidy. Previously, it was suggested that reduction of the MAD2 gene, encoding a major component of the SAC, induced aneuploidy in human tumor cells. However, tumor cell lines contain multiple mutations that might affect or exacerbate the cellular response to Mad2 depletion. Thus, the scenario resulting by Mad2 depletion in primary human cells could be different and more complex that the one depicted so far. We used primary human fibroblasts (IMR90) and epithelial breast cells (MCF10A) to gain further insight on the effects …

Genome instabilityCyclin-Dependent Kinase Inhibitor p21Cell cycle checkpointMad2PhysiologyClinical BiochemistryMAD2 depletion Aneuploidy Premature cellular senescence TP53Cell Cycle ProteinsBiologyCyclin-dependent kinaseChromosome instabilityChromosomal InstabilityTumor Suppressor Protein p14ARFHumansGene SilencingRNA Small InterferingMitosisCells CulturedCellular SenescenceCell ProliferationCalcium-Binding ProteinsCell BiologyCell Cycle CheckpointsFibroblastsAneuploidybeta-GalactosidaseCell biologyRepressor ProteinsSpindle checkpointSettore BIO/18 - GeneticaGene Expression RegulationMad2 Proteinsbiology.proteinM Phase Cell Cycle CheckpointsTumor Suppressor Protein p53Cell agingSignal Transduction
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High resistance to X-rays and therapeutic carbon ions in glioblastoma cells bearing dysfunctional ATM associates with intrinsic chromosomal instabili…

2014

To investigate chromosomal instability and radiation response mechanisms in glioblastoma cells.We undertook a comparative analysis of two patient-derived glioblastoma cell lines. Their resistance to low and high linear energy transfer (LET) radiation was assessed using clonogenic survival assay and their intrinsic chromosome instability status using fluorescence in situ hybridization. DNA damage was analyzed by pulsed-field gel electrophoresis and by γ-H2AX foci quantification. Expression of DNA damage response proteins was assessed by immunoblot.Increased radioresistance to X-rays as well as carbon ions was observed in glioblastoma cells exhibiting high levels of naturally occurring chromo…

Genome instabilityDNA RepairDNA damageLinear energy transferHeavy Ion RadiotherapyAtaxia Telangiectasia Mutated ProteinsBiologyRadiation ToleranceCell Line TumorChromosomal InstabilityRadioresistanceChromosome instabilitymedicineHumansDNA Breaks Double-StrandedLinear Energy TransferRadiology Nuclear Medicine and imagingGel electrophoresisRadiological and Ultrasound Technologymedicine.diagnostic_testX-RaysCell CycleGenomicsMolecular biologyPhosphorylationGlioblastomaSignal TransductionFluorescence in situ hybridizationInternational Journal of Radiation Biology
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Checkpoint adaptation in recombination-deficient cells drives aneuploidy and resistance to genotoxic agents.

2020

Abstract Human cancers frequently harbour mutations in DNA repair genes, rendering the use of DNA damaging agents as an effective therapeutic intervention. As therapy-resistant cells often arise, it is important to better understand the molecular pathways that drive resistance in order to facilitate the eventual targeting of such processes. We employ recombination-defective diploid yeast as a model to demonstrate that, in response to genotoxic challenges, nearly all cells eventually undergo checkpoint adaptation, resulting in the generation of aneuploid cells with whole chromosome losses that have acquired resistance to the initial genotoxic challenge. We demonstrate that adaptation inhibit…

Genome instabilitySaccharomyces cerevisiae ProteinsDNA RepairDNA repairAneuploidySaccharomyces cerevisiaeBiologyBiochemistryGenomic Instabilitychemistry.chemical_compoundGene Knockout TechniquesDrug Resistance FungalmedicineCytotoxicityMolecular BiologyRecombination GeneticSirolimusCell BiologyCell Cycle Checkpointsmedicine.diseaseAneuploidyPhenotypeDiploidyCell biologyRad52 DNA Repair and Recombination ProteinchemistryAdaptationPloidyDNADNA repair
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Long-Lasting Genomic Instability Following Arsenite Exposure inMammalian Cells: The Role of Reactive Oxygen Species

2011

Previously, we reported that the progeny of mammalian cells, which has been exposed to sodium arsenite for two cell cycles, exhibited chromosomal instability and concurrent DNA hypomethylation, when they were subsequently investigated after two months of subculturing (about 120 cell generations) in arsenite-free medium. In this work, we continued our investigations of the long-lasting arsenite-induced genomic instability by analyzing additional endpoints at several time points during the cell expanded growth. In addition to the progressive increase of aneuploid cells, we also noted micronucleated and multinucleated cells that continued to accumulate up to the 50th cell generation, as well a…

Genome instabilitySodium arseniteEpidemiologyArsenitesHealth Toxicology and MutagenesisPopulationCellarsenite; genomic instability; reactive oxygen speciesCHO CellsBiologyGenomic Instabilitychemistry.chemical_compoundMultinucleateCricetulusChromosome instabilityCricetinaemedicineAnimalseducationGenetics (clinical)Arseniteeducation.field_of_studyCell cycleDNA MethylationFlow CytometryMolecular biologyarseniteSettore BIO/18 - Geneticamedicine.anatomical_structurechemistryEnvironmental PollutantsReactive Oxygen Species
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Biological consequences of tumor hypoxia

2001

Growing evidence from experimental and clinical studies points to the fundamental, pathophysiologic role of hypoxia in solid tumors. Intratumoral hypoxia is a consequence of a structurally and functionally disturbed microcirculation, with deterioration of the diffusion geometry and of tumor-associated anemia. Hypoxia-induced changes of the proteome in the neoplastic and stroma cells may lead to neoplastic growth impairment through molecular mechanisms, resulting in cellular quiescence, differentiation, and apoptosis. Alternatively, hypoxia-induced proteome changes activating nonspecific stress response, anaerobic metabolism, angiogenesis, tissue remodeling, and change of cell contacts may p…

Genome instabilityStromal cellTumor hypoxiaAngiogenesisHematologyCell cycleHypoxia (medical)Biologymedicine.diseaseMetastasisOncologyImmunologyProteomeCancer researchmedicinemedicine.symptomSeminars in Oncology
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Physiological Mechanisms of Treatment Resistance

2009

It is generally accepted that tumor perfusion, microcirculation, characteristics of the interstitial space of tumors, oxygen (and nutrient) supply, tissue pH distribution and the bioenergetic status—factors that are usually closely linked and that define the so-called pathophysiological microenvironment—can markedly influence the therapeutic response of malignant tumors to sparsely ionizing radiation, chemotherapy, photodynamic therapy, hormonal therapy and immunotherapy. Besides more direct mechanisms involved in the development of acquired therapeutic resistance, there are in addition, obstacles in intratumor pharmacokinetics of antitumor agents due to delivery problems caused by an inade…

Genome instabilityTranscriptomeCell cycle checkpointInterstitial spacebusiness.industrymedicine.medical_treatmentmedicineCancer researchDistribution (pharmacology)Hormonal therapyImmunotherapybusinessMicrocirculation
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