Search results for "cycle"

showing 10 items of 3119 documents

Specific Irreversible Cell-Cycle Arrest and Depletion of Cancer Cells Obtained by Combining Curcumin and the Flavonoids Quercetin and Fisetin.

2022

Background: Induced senescence could be exploited to selectively counteract the proliferation of cancer cells and target them for senolysis. We examined the cellular senescence induced by curcumin and whether it could be targeted by fisetin and quercetin, flavonoids with senolytic activity. Methods: Cell-cycle profiles, chromosome number and structure, and heterochromatin markers were evaluated via flow cytometry, metaphase spreads, and immunofluorescence, respectively. The activation of p21waf1/cip1 was assessed via RT-qPCR and immunoblotting. Senescent cells were detected via SA-β-Galactosidase staining. Results: We report that curcumin treatment specifically triggers senescence in cancer…

Cyclin-Dependent Kinase Inhibitor p21FlavonoidsDNA methylationsenescenceCurcuminFlavonolsCell Cycle Checkpointssenescence; curcumin; senolytics; heterochromatin; DNA methylation; H3K9 trimethylation; SAHF; fisetin; quercetinSAHFSettore BIO/18 - GeneticaH3K9 trimethylationHeterochromatinNeoplasmssenolyticsGeneticsQuercetinGenetics (clinical)Genes
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Lovastatin causes sensitization of HeLa cells to ionizing radiation‐induced apoptosis by the abrogation of G2 blockage

2003

To investigate the effect of inhibition of Ras/Rho-regulated signalling by 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) on radiation-induced cell killing and apoptosis.Different human cell lines were pretreated or not with lovastatin before exposure to gamma-rays. Afterwards, radiation-induced cell killing, formation and repair of double-strand breaks, activation of radiation-inducible signal mechanisms (i.e. p53, p21, extracellular-signal-related kinase (ERK), NF-kappaB), changes in cell cycle progression and apoptosis were analysed.As shown by a colony formation assay, lovastatin sensitized HeLa cells to gamma-radiation-induced cell killing. The lovastati…

Cyclin-Dependent Kinase Inhibitor p21G2 PhaseMAPK/ERK pathwayApoptosisBiologyHeLaCyclinspolycyclic compoundsmedicineHumansRadiology Nuclear Medicine and imagingLovastatinSensitizationRadiological and Ultrasound TechnologyKinaseNF-kappa Bnutritional and metabolic diseasesCell cyclebiology.organism_classificationCell biologyCell killingmedicine.anatomical_structureGamma RaysApoptosislipids (amino acids peptides and proteins)LovastatinHydroxymethylglutaryl-CoA Reductase InhibitorsMitogen-Activated Protein KinasesTumor Suppressor Protein p53DNA DamageHeLa Cellsmedicine.drugInternational Journal of Radiation Biology
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Low doses of paclitaxel potently induce apoptosis in human retinoblastoma Y79 cells by up-regulating E2F1.

2008

Paclitaxel (PTX) is an anticancer drug currently in phase II clinical trials. This study shows for the first time that low doses of PTX (5 nM) potently induce apoptosis in human retinoblastoma Y79 cells. The effect of PTX is accompanied by a potent induction of E2F1 which appears to play a critical role in the effects induced by PTX. PTX induced a dose- and time-dependent effect, with G2/M arrest, cyclines A, E and B1 accumulation and a marked modification in the status of Cdc2-cyclin B1 complex, the major player of the G2/M checkpoint. Apoptosis followed G2/M arrest. An early and prolonged increase in p53 expression with its stabilization by phosphorylation and acetylation and its nuclear …

Cyclin-Dependent Kinase Inhibitor p21G2 Phaseendocrine systemCancer ResearchProgrammed cell deathPaclitaxelApoptosisBiologyretinoblastoma apoptosis paclitaxelp14arfSettore BIO/10 - BiochimicaCell Line TumorE2F1HumansFragmentation (cell biology)PhosphorylationMembrane Potential MitochondrialRetinoblastomaCell cycleAntineoplastic Agents PhytogenicUp-RegulationGene Expression Regulation NeoplasticOncologyApoptosisCancer researchPhosphorylationApoptosomeTumor Suppressor Protein p53Cell DivisionE2F1 Transcription FactorInternational journal of oncology
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Loss of Neuroglobin Expression Alters Cdkn1a/Cdk6-Expression Resulting in Increased Proliferation of Neural Stem Cells

2018

Abstract: In the quest to unravel its functional significance, neuroglobin (Ngb), a brain-specific neuroprotective protein, has recently been proposed as an actor in neurodevelopment. As neural stem cells (NSCs) are fundamental during brain development, the present study aimed at investigating the role of Ngb in the growth and proliferation of NSCs by comparing an Ngb-floxed (Ngb(fl)-)NSC line, equivalent to the wild-type cellular situation, with an in-house created Ngb knockout (Ngb(KO)-)NSC line. Ngb(KO)-NSCs were characterized by an increased growth and proliferation capacity in vitro, supported by RNA sequencing and western blot results reporting the downregulation of Cdkn1a and the upr…

Cyclin-Dependent Kinase Inhibitor p21Male0301 basic medicineCell signalingDown-RegulationNeuroglobinNerve Tissue ProteinsBiologyNeuroprotectionTranscriptomeMice03 medical and health sciences0302 clinical medicineNeural Stem CellsDownregulation and upregulationAnimalsBiologyCells CulturedCell ProliferationCell CycleCyclin-Dependent Kinase 6Cell BiologyHematologyCell cycleNeural stem cellUp-RegulationCell biologyMice Inbred C57BL030104 developmental biologynervous systemNeuroglobinbiology.proteinFemaleHuman medicineCyclin-dependent kinase 6Tumor Suppressor Protein p53Proto-Oncogene Proteins c-akt030217 neurology & neurosurgerySignal TransductionDevelopmental BiologyStem Cells and Development
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The structural plasticity of the C terminus of p21Cip1 is a determinant for target protein recognition.

2003

The cyclin-dependent kinase inhibitory protein p21(Cip1) might play multiple roles in cell-cycle regulation through interaction of its C-terminal domain with a defined set of cellular proteins such as proliferating cell nuclear antigen (PCNA), calmodulin (CaM), and the oncoprotein SET. p21(Cip1) could be described as an intrinsically unstructured protein in solution although the C-terminal domain adopts a well-defined extended conformation when bound to PCNA. However, the molecular mechanism of the interaction with CaM and the oncoprotein SET is not well understood, partly because of the lack of structural information. In this work, a peptide derived from the C-terminal domain of p21(Cip1) …

Cyclin-Dependent Kinase Inhibitor p21Models MolecularMagnetic Resonance SpectroscopyCalmodulinChromosomal Proteins Non-HistoneProtein ConformationPeptideBiologyLigandsBiochemistryBinding CompetitiveDomain (software engineering)Molecular recognitionCalmodulinCyclinsProliferating Cell Nuclear AntigenEscherichia coliHumansHistone ChaperonesMolecular Biologychemistry.chemical_classificationC-terminusCircular DichroismOrganic ChemistryCell CycleProteinsPeptide FragmentsCell biologyDNA-Binding ProteinschemistryBiochemistrybiology.proteinMolecular MedicineTarget proteinAlpha helixBinding domainTranscription FactorsChembiochem : a European journal of chemical biology
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The role of p21Waf1/CIP1 as a Cip/Kip type cell-cycle regulator in oral squamous cell carcinoma (Review)

2013

Oral Squamous Cell Carcinoma (OSCC) is biologically characterized by the accumulation of multiple genetic and molecular alterations that end up clinically characterized as a malignant neoplasm through a phenomenon known as multistep. The members of the Cip/Kip family, specifically p21 Waf 1/CIP1 , are responsible for cell cycle control, blocking the transition from phase G1 to phase S. We made a search of articles of peer-reviewed Journals in PubMed/ Medline, crossing the keywords. The goal of this paper is to determine the relationship between p21 Waf 1/ CIP1 expression and several clinical and pathological aspects of OSCC, their relationship with p53 and HPV, as well as genetic alteration…

Cyclin-Dependent Kinase Inhibitor p21Pathologymedicine.medical_specialtyRegulatorOdontologíaCarcinomamedicineBasal cellP21waf1 cip1General DentistryPathologicalMouth neoplasmOral Medicine and PathologyTransition (genetics)business.industryCell CycleReview-ArticleCell cyclemedicine.disease:CIENCIAS MÉDICAS [UNESCO]Ciencias de la saludstomatognathic diseasesOtorhinolaryngologyUNESCO::CIENCIAS MÉDICASCancer researchCarcinoma Squamous CellSurgeryMouth Neoplasmsbusiness
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Benzo[a]pyrene represses DNA repair through altered E2F1/E2F4 function marking an early event in DNA damage-induced cellular senescence

2020

AbstractTranscriptional regulation of DNA repair is of outmost importance for the restoration of DNA integrity upon genotoxic stress. Here we report that the potent environmental carcinogen benzo[a]pyrene (B[a]P) activates a cellular DNA damage response resulting in transcriptional repression of mismatch repair (MMR) genes (MSH2, MSH6, EXO1) and of RAD51, the central homologous recombination repair (HR) component, ultimately leading to downregulation of MMR and HR. B[a]P-induced gene repression is caused by abrogated E2F1 signalling. This occurs through proteasomal degradation of E2F1 in G2-arrested cells and downregulation of E2F1 mRNA expression in G1-arrested cells. Repression of E2F1-me…

Cyclin-Dependent Kinase Inhibitor p21SenescenceAcademicSubjects/SCI00010DNA repairDNA damageRAD51E2F4 Transcription FactorBiologyDNA Mismatch Repair03 medical and health sciences0302 clinical medicineCell Line TumorBenzo(a)pyreneGeneticsHumansCellular SenescenceCell Line Transformed030304 developmental biology0303 health sciencesGene regulation Chromatin and EpigeneticsRecombinational DNA RepairEpithelial CellsKv Channel-Interacting ProteinsCell Cycle CheckpointsDNAFibroblastsCell biologyDNA-Binding ProteinsRepressor ProteinsMSH6DNA Repair EnzymesExodeoxyribonucleasesMutS Homolog 2 ProteinGamma RaysMSH2030220 oncology & carcinogenesisCarcinogensMCF-7 CellsDNA mismatch repairRad51 RecombinaseCell agingE2F1 Transcription FactorDNA DamageSignal TransductionNucleic Acids Research
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Transcriptional repression of Bmp2 by p21(Waf1/Cip1) links quiescence to neural stem cell maintenance.

2013

Relative quiescence and self renewal are defining features of adult stem cells, but their potential coordination remains unclear. Subependymal neural stem cells (NSCs) lacking cyclin-dependent kinase (CDK) inhibitor (CKI) 1a (p21) exhibit rapid expansion that is followed by their permanent loss later in life. Here we demonstrate that transcription of the gene encoding bone morphogenetic protein 2 (Bmp2) in NSCs is under the direct negative control of p21 through actions that are independent of CDK. Loss of p21 in NSCs results in increased levels of secreted BMP2, which induce premature terminal differentiation of multipotent NSCs into mature non-neurogenic astrocytes in an autocrine and/or …

Cyclin-Dependent Kinase Inhibitor p21Time FactorsCellular differentiationBone Morphogenetic Protein 2Nerve Tissue ProteinsBiologyTransfectionParacrine signallingMiceNeural Stem CellsCyclin-dependent kinaseTransduction GeneticSubependymal zoneAnimalsCell Line TransformedRegulation of gene expressionMice KnockoutGeneral NeuroscienceNeurogenesisCell CycleAge FactorsCell DifferentiationNeural stem cellCell biologyKi-67 AntigenBromodeoxyuridineGene Expression RegulationMutagenesisCulture Media Conditionedbiology.proteinNeoplastic Stem CellsCarrier ProteinsNeuroscienceAdult stem cellSubcellular FractionsNature neuroscience
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A p16INK4a-insensitive CDK4 mutant targeted by cytolytic T lymphocytes in a human melanoma.

1995

A mutated cyclin-dependent kinase 4 (CDK4) was identified as a tumor-specific antigen recognized by HLA-A2. 1-restricted autologous cytolytic T lymphocytes (CTLs) in a human melanoma. The mutated CDK4 allele was present in autologous cultured melanoma cells and metastasis tissue, but not in the patient's lymphocytes. The mutation, an arginine-to-cysteine exchange at residue 24, was part of the CDK4 peptide recognized by CTLs and prevented binding of the CDK4 inhibitor p16INK4a, but not of p21 or of p27KIP1. The same mutation was found in one additional melanoma among 28 melanomas analyzed. These results suggest that mutation of CDK4 can create a tumor-specific antigen and can disrupt the ce…

Cyclin-Dependent Kinase Inhibitor p21Tumor suppressor geneMutantMolecular Sequence DataCell Cycle ProteinsBiologyProtein Serine-Threonine Kinasesmedicine.disease_causeTransfectionPolymerase Chain ReactionMetastasisCell LineAntigenCyclinsProto-Oncogene ProteinsHLA-A2 AntigenmedicineTumor Cells CulturedAnimalsHumansPoint MutationAmino Acid SequenceCloning MolecularneoplasmsMelanomaCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p15MutationMultidisciplinaryintegumentary systemBase SequenceMelanomaTumor Suppressor ProteinsCyclin-Dependent Kinase 4Cell cyclemedicine.diseaseCyclin-Dependent KinasesCytolysisCancer researchCarrier ProteinsMicrotubule-Associated ProteinsCyclin-Dependent Kinase Inhibitor p27T-Lymphocytes CytotoxicScience (New York, N.Y.)
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1,2,3-Triazole in Heterocyclic Compounds, Endowed with Biological Activity, through 1,3-Dipolar Cycloadditions

2014

1,3-Dipolar cycloaddition reactions can be considered a powerful synthetic tool in the building of heterocyclic rings, with applications in different fields. In this review we focus on the synthesis of biologically active compounds possessing the 1,2,3-triazole core through 1,3-dipolar cycloaddition reactions. The 1,2,3-triazole skeleton can be present as a single disubstituted ring, as a linker between two molecules, or embedded in a polyheterocycle. The cycloaddition reactions are usually catalysed by copper or ruthenium. Domino reactions can be achieved through dipolarophile anion formation, generally followed by cyclisation. The variety of attainable heterocyclic structures gives an ill…

Cycloaddition / Nitrogen heterocycles / Domino reactions / Homogeneous catalysis / Enzyme catalysis / Biological activity / Medicinal chemistrySettore CHIM/03 - Chimica Generale E InorganicaCycloaddition Nitrogen heterocycles Domino reactions Homogeneous catalysis Enzyme catalysis Biological activity Medicinal chemistrySettore CHIM/08 - Chimica Farmaceutica
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