Search results for "SENESCENCE"

showing 10 items of 339 documents

Compromised nuclear envelope integrity drives tumor cell invasion

2020

AbstractWhile mutations leading to a fragile envelope of the cell nucleus are well known to cause diseases such as muscular dystrophies or accelerated aging, the pathophysiological consequences of the recently discovered mechanically induced nuclear envelope ruptures in cells harboring no mutation are less known. Here we show that repeated loss of nuclear envelope integrity in nuclei experiencing mechanical constraints promotes senescence in nontransformed cells, and induces an invasive phenotype including increased collagen degradation in human breast cancer cells, both in vitro and in a mouse xenograft model of breast cancer progression. We show that these phenotypic changes are due to th…

SenescenceCell nucleusMutationmedicine.anatomical_structureCytoplasmChemistryDNA damageCancer cellmedicinemedicine.disease_causePhenotypeExtracellular Matrix DegradationCell biology
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DNA damage causes TP53-dependent coupling of self-renewal and senescence pathways in embryonal carcinoma cells.

2013

Recent studies have highlighted an apparently paradoxical link between self-renewal and senescence triggered by DNA damage in certain cell types. In addition, the finding that TP53 can suppress senescence has caused a re-evaluation of its functional role in regulating these outcomes. To investigate these phenomena and their relationship to pluripotency and senescence, we examined the response of the TP53-competent embryonal carcinoma (EC) cell line PA-1 to etoposide-induced DNA damage. Nuclear POU5F1/OCT4A and P21CIP1 were upregulated in the same cells following etoposide-induced G 2M arrest. However, while accumulating in the karyosol, the amount of OCT4A was reduced in the chromatin fract…

SenescenceCyclin-Dependent Kinase Inhibitor p21OCT4A/POU5F1Embryonal Carcinoma Stem CellssenescenceDNA RepairDNA repairDNA damagetumor cellsBiologyProtein Serine-Threonine Kinasesself-renewalHistonesAurora KinasesCell Line TumorReportAutophagyAurora Kinase BHumansTP53PhosphorylationRNA Small InterferingMolecular BiologyMitosisCellular SenescenceCyclin-Dependent Kinase Inhibitor p16EtoposideOvarian NeoplasmsEmbryonal Carcinoma Stem CellsCell BiologyG2-M DNA damage checkpointbeta-GalactosidasepluripotencyAntineoplastic Agents PhytogenicChromatinUp-RegulationG2 Phase Cell Cycle CheckpointsCheckpoint Kinase 2Cancer researchDNA damageFemaleRNA InterferenceRad51 RecombinaseTumor Suppressor Protein p53Cell agingOctamer Transcription Factor-3Developmental BiologyCell cycle (Georgetown, Tex.)
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Oxidative Stress and the Epigenetics of Cell Senescence: Insights from Progeroid Syndromes.

2019

Background: Cell senescence constitutes a critical process to respond to a variety of insults and adverse circumstances. Senescence involves the detention of DNA replication and cell proliferation, and hence, genetic programs associated with DNA damage response, chromosome stability, chromatin rearrangement, epigenetic reprogramming, and cell cycle are tightly linked to the senescent phenotype. Although senescence increases with age, the real implication of senescence regulation in the progress of aging in humans is largely discussed. In this context, reactive oxygen species (ROS) accumulation has also been postulated to play a critical role in cell homeostasis, aging processes, and contro…

SenescenceDNA damageContext (language use)Biology01 natural sciencesProgeroid syndromesEpigenesis Genetic03 medical and health sciencesDrug DiscoverymedicineAnimalsHumansEpigeneticsCellular Senescence030304 developmental biologyPharmacology0303 health sciencesSyndromeCell cyclemedicine.disease0104 chemical sciencesChromatinCell biology010404 medicinal & biomolecular chemistryOxidative StressReactive Oxygen SpeciesReprogrammingCurrent pharmaceutical design
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Down-Regulation of Ku Autoantigen, DNA-Dependent Protein Kinase, and Poly(ADP-ribose) Polymerase during Cellular Senescence

1997

During aging and cellular senescence mutations accumulate in genomic and mitochondrial DNA. Ku autoantigens, DNA-dependent protein kinase, and poly (ADP-ribose) polymerase have an essential role in DNA damage recognition. Our purpose was to find out whether cellular senescence of fibroblasts affects the protein components that recognize DNA damage and induce the repair process. We compared presenescent and replicatively senescent human WI-38 fibroblasts with each other and with SV-40 immortalized and serum-deficient quiescent WI-38 cells. Our results showed that replicative senescence significantly decreased the nuclear level of both p70 and p86 components of Ku autoantigen. SV-40 immortali…

SenescenceDNA damagePoly ADP ribose polymeraseMolecular Sequence DataBiophysicsDown-RegulationP70-S6 Kinase 1DNA FragmentationDNA-Activated Protein KinaseProtein Serine-Threonine KinasesAutoantigensBiochemistryCell LineDownregulation and upregulationHumansAmino Acid SequenceProtein kinase AKu AutoantigenLungMolecular BiologyCellular SenescencePolymerasebiologyDNA HelicasesNuclear ProteinsAntigens NuclearCell BiologyFibroblastsMolecular biologyDNA-Binding ProteinsApoptosisbiology.proteinPoly(ADP-ribose) PolymerasesBiochemical and Biophysical Research Communications
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SGLT2i and GLP-1RA in Cardiometabolic and Renal Diseases: From Glycemic Control to Adipose Tissue Inflammation and Senescence

2021

Background. Over the last few years, the use of sodium-glucose cotransporter 2 inhibitors (SGLT2i) and glucagon-like peptide 1 receptor agonists (GLP-1RA) has increased substantially in medical practice due to their documented benefits in cardiorenal and metabolic health. In this sense, and in addition to being used for glycemic control in diabetic patients, these drugs also have other favorable effects such as weight loss and lowering blood pressure, and more recently, they have been shown to have cardio and renoprotective effects with anti-inflammatory properties. Concerning the latter, the individual or associated use of these antihyperglycemic agents has been linked with a decrease in p…

SenescenceEndocrinology Diabetes and MetabolismAdipose tissueInflammationGlycemic ControlReview ArticleDiseaseBioinformaticsDiseases of the endocrine glands. Clinical endocrinologyGlucagon-Like Peptide-1 ReceptorProinflammatory cytokineEndocrinologySodium-glucose cotransporter 2 inhibitors (SGLT2i)Weight lossDiabetes mellitusmedicineHumansSodium-Glucose Transporter 2 InhibitorsCellular SenescenceGlycemicInflammationMetabolic SyndromeManagement of diabetesRonyonsDiabetisbusiness.industryRC648-665medicine.diseaseCor MalaltiesAdipose TissueantihyperglycemicPatients obesity and cardiorenal compromiseglycemic controlmedicine.symptombusinessGlucagon-like peptide 1 receptor agonists (GLP-1RA)
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Compromised nuclear envelope integrity drives TREX1-dependent DNA damage and tumor cell invasion

2021

Although mutations leading to a compromised nuclear envelope cause diseases such as muscular dystrophies or accelerated aging, the consequences of mechanically induced nuclear envelope ruptures are less known. Here, we show that nuclear envelope ruptures induce DNA damage that promotes senescence in non-transformed cells and induces an invasive phenotype in human breast cancer cells. We find that the endoplasmic reticulum (ER)-associated exonuclease TREX1 translocates into the nucleus after nuclear envelope rupture and is required to induce DNA damage. Inside the mammary duct, cellular crowding leads to nuclear envelope ruptures that generate TREX1-dependent DNA damage, thereby driving the …

SenescenceExonucleaseDNA damageNuclear Envelope[SDV]Life Sciences [q-bio]Breast NeoplasmsBiologySettore MED/08 - Anatomia PatologicaGeneral Biochemistry Genetics and Molecular BiologyCell LineMicemedicineSettore MED/05 - Patologia ClinicaAnimalsHumansNeoplasm InvasivenessEpithelial–mesenchymal transitionCellular SenescenceEndoplasmic reticulumPhosphoproteinsXenograft Model Antitumor AssaysCell biology[SDV] Life Sciences [q-bio]medicine.anatomical_structureExodeoxyribonucleasesCancer cellProteolysisbiology.proteinTREX1 nuclear envelope rupture DNA damage mammary duct carcinoma tumor invasion senescence breast cancer cGAS confinement epithelial to mesenchymal transition Animals Breast Neoplasms Cell Line Cellular Senescence Collagen Disease Progression Exodeoxyribonucleases Female Humans Mice Neoplasm InvasivenessNuclear Envelope PhosphoproteinsProteolysis Xenograft Model Antitumor Assays DNA DamageDisease ProgressionFemaleCollagenNucleusExtracellular Matrix DegradationDNA Damage
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Changes in the Level of Peptidase Activities in Pea Ovaries during Senescence and Fruit Set Induced by Gibberellic Acid

1990

The activities and changes in the levels of exopeptidase and endopeptidase activities were characterized in unpollinated ovaries of Pisum sativum L. cv Alaska during senescence and early fruit development induced by gibberellic acid (GA3). Two aminopeptidases and one iminopeptidase were electrophoretically separated. These peptidases were sensitive to inhibitors of sulfhydryl proteases. Carboxypeptidase activity was inhibited by phenylmethyl sulfonyl fluoride. An azocasein-degrading endopeptidase, sensitive to thiol protease inhibitors, was also found. An increase in the specific activity of aminopeptidase during both fruit development and ovary senescence was observed. In contrast, the spe…

SenescenceExopeptidase activityPhysiologyfood and beveragesPlant ScienceBiologyExopeptidaseCarboxypeptidaseEndopeptidaseCarboxypeptidase activityEndopeptidase activityBiochemistryGeneticsbiology.proteinGibberellinPlant Physiology
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Telomere length and cardiovascular disease

2010

SummaryTelomeres are structures composed of deoxyribonucleic acid repeats that protect the end of chromosomes, but shorten with each cell division. They have been the subject of many studies, particularly in the field of oncology, and more recently their role in the onset, development and prognosis of cardiovascular disease has generated considerable interest. It has already been shown that these structures may deteriorate at the beginning of the atherosclerotic process, in the onset and development of arterial hypertension or during myocardial infarction, in which their length may be a predictor of outcome. As telomere length by its nature is a marker of cell senescence, it is of particula…

SenescenceGenetic Markersmedicine.medical_specialtyCell divisionDiseaseBioinformaticsmedicine.disease_causeTélomèreInternal medicinemedicineAnimalsHumansFacteurs de risque cardiovasculairesMyocytes CardiacMyocardial infarctionRisk factorCellular SenescenceCardiovascular risk factorsMaladies cardiovasculairesbusiness.industryStress oxydatifGeneral MedicineTelomeremedicine.diseaseTelomereEndocrinologyCardiovascular diseasesGene Expression RegulationGenetic markerOxidative stressEndothelium VascularbusinessCardiology and Cardiovascular MedicineOxidative stressArchives of Cardiovascular Diseases
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The dual role of p53: DNA protection and antioxidant.

2011

The classical functions of p53 protein are those related to its role on DNA damage, cell growth arrest, senescence and apoptosis. For this reason it is called 'the guardian of the genome' and is considered one of the most important players in the development of cancer. However, more recently it has been show that p53 is not only involved in cancer, but also in ageing. p53 is stimulated by stress, which in turn results in the activation of a wide range of transcriptional targets. Low-intensity stress will activate p53 in a manner which results in antioxidant response, thus protecting against ageing because of its antioxidant function. On the contrary, high-intensity activation of p53 will re…

SenescenceGenome instabilityDNA protectionAgingDNA damageBiologymedicine.disease_causeBiochemistryAntioxidantsGenomic InstabilityNeoplasmsmedicineAnimalsHumansCellular SenescenceHeat-Shock ProteinsCell growthCell CycleGeneral MedicineCell cycleCell biologyBiochemistryAgeingTumor Suppressor Protein p53Reactive Oxygen SpeciesOxidative stressFree radical research
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Effect of aging on glutathione metabolism. Protection by antioxidants

1992

The free radical, theory of aging suggests that oxygen free radicals may be involved in the aging process. Thus, changes in antioxidant mechanisms may occur with aging. Since glutathione is one of the most effective antioxidant systems in the cell, its metabolism may change with aging. In this chapter we describe experiments which show the involvement of glutathione in the aging process and which provide a rationale for the administration of antioxidants to old organisms to protect them against some of the changes that occur with aging.

SenescenceGlutathione metabolismAntioxidantRadicalmedicine.medical_treatmentMetabolismGlutathionechemistry.chemical_compoundchemistryBiochemistrymedicineGlutathione disulfidesense organsskin and connective tissue diseasesFree-radical theory of aging
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