Search results for "Instability"

showing 10 items of 724 documents

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
researchProduct

Inactivation of folylpolyglutamate synthetase Met7 results in genome instability driven by an increased dUTP/dTTP ratio

2020

AbstractThe accumulation of mutations is frequently associated with alterations in gene function leading to the onset of diseases, including cancer. Aiming to find novel genes that contribute to the stability of the genome, we screened the Saccharomyces cerevisiae deletion collection for increased mutator phenotypes. Among the identified genes, we discovered MET7, which encodes folylpolyglutamate synthetase (FPGS), an enzyme that facilitates several folate-dependent reactions including the synthesis of purines, thymidylate (dTMP) and DNA methylation. Here, we found that Met7-deficient strains show elevated mutation rates, but also increased levels of endogenous DNA damage resulting in gross…

Genome instabilityCell- och molekylärbiologiSaccharomyces cerevisiaeGenome Integrity Repair and ReplicationBiologymedicine.disease_causeGenomic InstabilityFolic AcidGene Expression Regulation FungalGeneticsmedicineThymine NucleotidesPeptide SynthasesDNA FungalUracilGeneCell NucleusRegulation of gene expressionMutationFolylpolyglutamate synthaseFungal geneticsDeoxyguanine NucleotidesMutation AccumulationMolecular biologyMitochondriaMutationDNA methylationGenome FungalDeoxyuracil NucleotidesGene DeletionCell and Molecular BiologyDNA Damage
researchProduct

7E olfactory receptor gene clusters and evolutionary chromosome rearrangements

2005

Olfactory receptor (OR) genes of the 7E subfamily have been duplicated to multiple regions throughout the human genome. Segmental duplications containing 7E OR genes have been associated with both pathological and evolutionary chromosome rearrangements. Many of these breakpoint regions coincide with breaks of chromosomal synteny in the mouse, rat and/or chicken genomes. Collectively, these data suggest that 7E OR-containing regions represent hot spots of genomic instability.    

Genome instabilityChromosomes Artificial BacterialGenome evolutionBiologyReceptors OdorantGenomeEvolution MolecularGene DuplicationGeneticsmedicineAnimalsHumansMolecular BiologyGeneIn Situ Hybridization FluorescenceGenetics (clinical)SyntenySegmental duplicationGene RearrangementMammalsGeneticsGenomeOlfactory receptorGenome HumanChromosome Mappingmedicine.anatomical_structureMultigene FamilyHuman genomeCytogenetic and Genome Research
researchProduct

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
researchProduct

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
researchProduct

Hypoxia and Human Genome Stability: Downregulation of BRCA2 Expression in Breast Cancer Cell Lines

2013

Previously, it has been reported that hypoxia causes increased mutagenesis and alteration in DNA repair mechanisms. In 2005, an interesting study showed that hypoxia-induced decreases in BRCA1 expression and the consequent suppression of homologous recombination may lead to genetic instability. However, nothing is yet known about the involvement of BRCA2 in hypoxic conditions in breast cancer. Initially, a cell proliferation assay allowed us to hypothesize that hypoxia could negatively regulate the breast cancer cell growth in short term in vitro studies. Subsequently, we analyzed gene expression in breast cancer cell lines exposed to hypoxic condition by microarray analysis. Interestingly,…

Genome instabilityDNA RepairArticle SubjectDNA repairDNA damageSettore MED/06 - Oncologia MedicaDown-Regulationlcsh:MedicineBreast NeoplasmsBiologyGeneral Biochemistry Genetics and Molecular BiologyGenomic InstabilityBreast cancerCell Line TumorBreast CancermedicineHumansEnzyme Inhibitorsskin and connective tissue diseasesHypoxiaBiologyGeneral Immunology and MicrobiologyBRCA1 ProteinGenome Humanlcsh:RGenome StabilityGeneral MedicineDNA repair protein XRCC4medicine.diseaseBRCA2Cell HypoxiaAmino Acids DicarboxylicGene Expression Regulation NeoplasticCancer researchDNA mismatch repairFemaleHuman medicineHypoxia; Genome Stability; BRCA2; Breast CancerHomologous recombinationEngineering sciences. TechnologyNucleotide excision repairResearch ArticleDNA Damage
researchProduct

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
researchProduct

Humans and chimpanzees differ in their cellular response to DNA damage and non-coding sequence elements of DNA repair-associated genes.

2008

Compared to humans, chimpanzees appear to be less susceptible to many types of cancer. Because DNA repair defects lead to accumulation of gene and chromosomal mutations, species differences in DNA repair are one plausible explanation. Here we analyzed the repair kinetics of human and chimpanzee cells after cisplatin treatment and irradiation. Dot blots for the quantification of single-stranded (ss) DNA repair intermediates revealed a biphasic response of human and chimpanzee lymphoblasts to cisplatin-induced damage. The early phase of DNA repair was identical in both species with a peak of ssDNA intermediates at 1 h after DNA damage induction. However, the late phase differed between specie…

Genome instabilityDNA RepairPan troglodytesDNA damageDNA repairBiologychemistry.chemical_compoundExtrachromosomal DNAGeneticsCoding regionAnimalsHumansLymphocytesRNA MessengerMolecular BiologyGeneGenetics (clinical)Cells CulturedGeneticsBase SequenceDNAchemistryHuman genomeCisplatinDNADNA DamageCytogenetic and genome research
researchProduct

<i>MYC</i> Dosage Compensation is Mediated by miRNA-Transcription Factor Interactions in Aneuploid Cancer

2021

Cancer complexity is consequence of genomic instability leading to aneuploidy. We hypothesize that dosage compensation of critical genes arise from systems-level properties for cancer cells to withstand the negative effects of aneuploidy. We developed a computational platform to identify a network of miRNAs and transcription factors interacting with candidate dosage-compensated genes using NCI-60 multi-omic data. We next constructed a mathematical model where the property of dosage compensation emerged for MYC and STAT3 and was dependent on the kinetic parameters of their feedback and feed-forward interactions with four miRNAs. We developed a genetic tug-of-war approach by overexpressing an…

Genome instabilityDosage compensationColorectal cancermicroRNACancer cellCancer researchmedicineCancerBiologymedicine.diseaseGene dosageTranscription factorSSRN Electronic Journal
researchProduct

MYC dosage compensation is mediated by miRNA-transcription factor interactions in aneuploid cancer

2021

SummaryWe hypothesize that dosage compensation of critical genes arises from systems-level properties for cancer cells to withstand the negative effects of aneuploidy. We identified several candidate genes in cancer multi-omics data and developed a biocomputational platform to construct a mathematical model of their interaction network with miRNAs and transcription factors, where the property of dosage compensation emerged for MYC and was dependent on the kinetic parameters of its feedback interactions with three micro-RNAs. These circuits were experimentally validated with a novel genetic tug-of-war technique by overexpressing an exogenous MYC leading to over-expression of the three microR…

Genome instabilityDosage compensationColorectal cancermicroRNACancer cellmedicineCancer researchCancerBiologymedicine.diseaseGene dosageTranscription factor
researchProduct