Search results for "Cyclin-Dependent Kinase Inhibitor p21"

showing 3 items of 33 documents

Cytotoxic Activity of Organotin(IV) Derivatives with Triazolopyrimidine Containing Exocyclic Oxygen Atoms

2020

In this study cytotoxicity of organotin(IV) compounds with 1,2,4-triazolo[1,5-a]pyrimidines, Me3Sn(5tpO) (1), n-Bu3Sn(5tpO) (2), Me3Sn(mtpO) (3), n-Bu3Sn(mtpO) (4), n-Bu3Sn(HtpO2) (5), Ph3Sn(HtpO2) (6) where 5HtpO = 4,5-dihydro-5-oxo-[1,2,4]triazolo-[1,5-a]pyrimidine, HmtpO = 4,7-dihydro-5-methyl-7-oxo-[1,2,4]triazolo-[1,5-a]pyrimidine, and H2tpO2 = 4,5,6,7-tetrahydro-5,7- dioxo-[1,2,4]triazolo-[1,5-a]-pyrimidine, was assessed on three different human tumor cell lines: HCT-116 (colorectal carcinoma), HepG2 (hepatocarcinoma) and MCF-7 (breast cancer). While 1 and 3 were inactive, compounds 2, 4, 5 and 6 inhibited the growth of the three tumor cell lines with IC50 values in the submicromolar …

DenticityCellPharmaceutical Science01 natural sciencesAnalytical Chemistrychemistry.chemical_compoundDrug DiscoveryOrganotin CompoundstriazolopyrimidineCytotoxicityMembrane Potential MitochondrialCytotoxinsapoptosisBiological activityHep G2 CellsG2 Phase Cell Cycle CheckpointsGene Expression Regulation Neoplasticmedicine.anatomical_structureChemistry (miscellaneous)Mitochondrial MembranesMCF-7 CellsMolecular MedicineCyclin-Dependent Kinase Inhibitor p21crystal structurein vitro anticancer activityPyrimidineCell SurvivalStereochemistryorganotin(iv)010402 general chemistryArticlelcsh:QD241-441Inhibitory Concentration 50Structure-Activity Relationshiplcsh:Organic chemistrymedicineHumansPhysical and Theoretical ChemistryMetallodrug010405 organic chemistryLigandOrganic ChemistryTriazolesHCT116 CellsapoptosiG1 Phase Cell Cycle Checkpoints0104 chemical sciencesPyrimidineschemistrymetallodrugsCell cultureApoptosisDrug DesignTumor Suppressor Protein p53Reactive Oxygen SpeciesMolecules
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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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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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