Search results for "Cell cycle"

showing 10 items of 804 documents

Telomere Length Determines TERRA and R-Loop Regulation through the Cell Cycle

2017

Maintenance of a minimal telomere length is essential to prevent cellular senescence. When critically short telomeres arise in the absence of telomerase, they can be repaired by homology-directed repair (HDR) to prevent premature senescence onset. It is unclear why specifically the shortest telomeres are targeted for HDR. We demonstrate that the non-coding RNA TERRA accumulates as HDR-promoting RNA-DNA hybrids (R-loops) preferentially at very short telomeres. The increased level of TERRA and R-loops, exclusively at short telomeres, is due to a local defect in RNA degradation by the Rat1 and RNase H2 nucleases, respectively. Consequently, the coordination of TERRA degradation with telomere r…

0301 basic medicineSenescenceTelomeraseSaccharomyces cerevisiae ProteinssenescenceDNA damageR-loopTelomere-Binding ProteinsSaccharomyces cerevisiaeBiologyDDRGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesRif2Cellular SenescenceTelomere-binding proteinRNA-DNA hybridtelomereBiochemistry Genetics and Molecular Biology (all)Telomere-Binding ProteinCell CycleRNANucleic Acid HybridizationRecombinational DNA RepairTERRARepressor ProteinMolecular biologyRat1ExoribonucleaseTelomereRepressor Proteins030104 developmental biologyCell AgingExoribonucleasesR-loopRNase H2Cell agingSaccharomyces cerevisiae ProteinDNA Damage
researchProduct

Cytotoxicity of seven naturally occurring phenolic compounds towards multi-factorial drug-resistant cancer cells

2016

Abstract Introduction In medical oncology, multi-drug resistance (MDR) of cancer cells continues to be a major impediment. We are in quest of novel anti-proliferative agents to overcome drug-resistant tumor cells. Methods In the present study, we investigated the cytotoxicity of 7 naturally occurring phenolic compounds including two isoflavonoids alpinumisoflavone ( 1 ) and laburnetin ( 2 ), one biflavonoid amentoflavone ( 3) , three lignans pycnanthulignene A ( 4 ), pycnanthulignene B ( 5 ), and syringaresinol ( 7 ) and one xanthone, euxanthone ( 6 ) against 9 drug-sensitive and MDR cancer cell lines. The resazurin reduction assay was used to evaluate the cytotoxicity of these compounds, w…

0301 basic medicineSyringaresinolPharmaceutical SciencePharmacologyAmentoflavone03 medical and health scienceschemistry.chemical_compound0302 clinical medicinePhenolsIsoflavonoidCell Line TumorNeoplasmsOxazinesDrug DiscoveryHumansCytotoxic T cellCytotoxicityMembrane Potential MitochondrialPharmacologyCell Cycle CheckpointsAlpinumisoflavoneAntineoplastic Agents PhytogenicDrug Resistance MultipleEnzyme Activation030104 developmental biologyXanthenesComplementary and alternative medicinechemistryDrug Resistance NeoplasmApoptosisCaspases030220 oncology & carcinogenesisCancer cellMolecular MedicineReactive Oxygen SpeciesPhytomedicine
researchProduct

One-Cell Doubling Evaluation by Living Arrays of Yeast, ODELAY!

2016

Abstract Cell growth is a complex phenotype widely used in systems biology to gauge the impact of genetic and environmental perturbations. Due to the magnitude of genome-wide studies, resolution is often sacrificed in favor of throughput, creating a demand for scalable, time-resolved, quantitative methods of growth assessment. We present ODELAY (One-cell Doubling Evaluation by Living Arrays of Yeast), an automated and scalable growth analysis platform. High measurement density and single-cell resolution provide a powerful tool for large-scale multiparameter growth analysis based on the modeling of microcolony expansion on solid media. Pioneered in yeast but applicable to other colony formin…

0301 basic medicineSystems biologySaccharomyces cerevisiaeCellBioengineeringSaccharomyces cerevisiaeInvestigationsBiologyyeastQH426-470lag time03 medical and health sciencesGenetic HeterogeneityLag timeSingle-cell analysismedicinePopulation Heterogeneitycarrying capacityGeneticsDoubling timeMolecular BiologyThroughput (business)Genetics (clinical)030304 developmental biologyCell Proliferation0303 health sciencesGenomeEcology030306 microbiologyCell growthSystems BiologyCell CycleHuman Genomebiology.organism_classificationYeast030104 developmental biologymedicine.anatomical_structurePhenotypeFungalGene-Environment Interactiongrowth ratefitness assessmentGeneric health relevanceGenome FungalSingle-Cell AnalysisBiological systemG3: Genes, Genomes, Genetics
researchProduct

Characterizing diversity in the tumor-immune microenvironment of distinct subclasses of gastroesophageal adenocarcinomas

2020

Background Gastroesophageal adenocarcinomas (GEAs) are heterogeneous cancers where immune checkpoint inhibitors have robust efficacy in heavily inflamed microsatellite instability (MSI) or Epstein-Barr virus (EBV)-positive subtypes. Immune checkpoint inhibitor responses are markedly lower in diffuse/genome stable (GS) and chromosomal instable (CIN) GEAs. In contrast to EBV and MSI subtypes, the tumor microenvironment of CIN and GS GEAs have not been fully characterized to date, which limits our ability to improve immunotherapeutic strategies. Patients and methods Here we aimed to identify tumor-immune cell association across GEA subclasses using data from The Cancer Genome Atlas (N = 453 GE…

0301 basic medicineT cellmedicine.medical_treatmentAdenocarcinomaArticle03 medical and health sciences0302 clinical medicineImmune systemStomach NeoplasmsTumor MicroenvironmentMedicineHumansTumor microenvironmentbusiness.industryMicrosatellite instabilityHematologyImmunotherapyCell cyclemedicine.diseaseImmunohistochemistry030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisCancer researchAdenocarcinomaMicrosatellite InstabilitybusinessCD8
researchProduct

Acute depletion of telomerase components DKC1 and NOP10 induces oxidative stress and disrupts ribosomal biogenesis via NPM1 and activation of the P53…

2020

Mutations in DKC1, NOP10, and TINF2 genes, coding for proteins in telomerase and shelterin complexes, are responsible for diverse diseases known as telomeropathies and ribosomopathies, including dyskeratosis congenita (DC, ORPHA 1775). These genes contribute to the DC phenotype through mechanisms that are not completely understood. We previously demonstrated in models of DC that oxidative stress is an early and independent event that occurs prior to telomere shortening. To clarify the mechanisms that induce oxidative stress, we silenced genes DKC1, NOP10, and TINF2 with siRNA technology. With RNA array hybridisation, we found several altered pathways for each siRNA model. Afterwards, we ide…

0301 basic medicineTelomeraseTelomere-Binding ProteinsCell Cycle ProteinsShelterin ComplexCell LineAdherens junction03 medical and health sciences0302 clinical medicineRibonucleoproteins Small NucleolarmedicineRNA Small InterferingMolecular BiologyTelomeraseTelomere ShorteningRibonucleoproteinChemistryRNANuclear ProteinsCell BiologyTelomereShelterinmedicine.diseaseCell biologyTelomereOxidative Stress030104 developmental biology030220 oncology & carcinogenesisMutationTumor Suppressor Protein p53NucleophosminRibosomesDyskeratosis congenitaBiogenesisBiochimica et biophysica acta. Molecular cell research
researchProduct

Dom34 Links Translation to Protein O-mannosylation.

2016

In eukaryotes, Dom34 upregulates translation by securing levels of activatable ribosomal subunits. We found that in the yeast Saccharomyces cerevisiae and the human fungal pathogen Candida albicans, Dom34 interacts genetically with Pmt1, a major isoform of protein O-mannosyltransferase. In C. albicans, lack of Dom34 exacerbated defective phenotypes of pmt1 mutants, while they were ameliorated by Dom34 overproduction that enhanced Pmt1 protein but not PMT1 transcript levels. Translational effects of Dom34 required the 5′-UTR of the PMT1 transcript, which bound recombinant Dom34 directly at a CA/AC-rich sequence and regulated in vitro translation. Polysomal profiling revealed that Dom34 stimu…

0301 basic medicineUntranslated regionCancer ResearchGlycosylationMolecular biologyHydrolasesOligonucleotidesGene ExpressionRNA-binding proteinCell Cycle ProteinsYeast and Fungal ModelsPathology and Laboratory MedicineMannosyltransferasesBiochemistryTranscription (biology)Untranslated RegionsCandida albicansMedicine and Health SciencesProtein IsoformsGenetics (clinical)CandidaFungal PathogensNucleotidesMessenger RNACell biologyEnzymesNucleic acidsDenaturationPhenotypesPhenotypeMedical MicrobiologySaccharomyces CerevisiaePathogensResearch ArticleGene isoformSaccharomyces cerevisiae Proteinslcsh:QH426-470NucleasesSaccharomyces cerevisiaeMycologyBiologyResearch and Analysis MethodsMicrobiology03 medical and health sciencesSaccharomycesModel OrganismsRibonucleasesDownregulation and upregulationEndoribonucleasesDNA-binding proteinsGeneticsHumansGeneMicrobial PathogensEcology Evolution Behavior and Systematics030102 biochemistry & molecular biologyOrganismsFungiBiology and Life SciencesProteinsRibosomal RNAbiology.organism_classificationMolecular biologyYeastRNA denaturationlcsh:Genetics030104 developmental biologyMolecular biology techniquesProtein BiosynthesisEnzymologyRNAProtein TranslationRibosomesPLoS Genetics
researchProduct

Impact of the Usher syndrome on olfaction

2015

Usher syndrome is a genetically and clinically heterogeneous disease in humans, characterized by sensorineural hearing loss, retinitis pigmentosa and vestibular dysfunction. This disease is caused by mutations in genes encoding proteins that form complex networks in different cellular compartments. Currently, it remains unclear whether the Usher proteins also form networks within the olfactory epithelium (OE). Here, we describe Usher gene expression at the mRNA and protein level in the OE of mice and showed interactions between these proteins and olfactory signaling proteins. Additionally, we analyzed the odor sensitivity of different Usher syndrome mouse models using electro-olfactogram re…

0301 basic medicineUsher syndromeCell Cycle ProteinsMice TransgenicNerve Tissue ProteinsOlfactionMyosinsBiologyCell LineMice03 medical and health sciencesOlfactory MucosaGene expressionRetinitis pigmentosaotorhinolaryngologic diseasesGeneticsmedicineAnimalsHumansCiliaMolecular BiologyGeneGenetics (clinical)GeneticsExtracellular Matrix ProteinsMessenger RNAGene Expression ProfilingEpithelial CellsGeneral MedicineCadherinsmedicine.diseaseeye diseasesSmellCytoskeletal ProteinsDisease Models Animal030104 developmental biologymedicine.anatomical_structureGene Expression RegulationMyosin VIIaMutationOdorantsSignal transductionCarrier ProteinsUsher SyndromesOlfactory epitheliumSignal TransductionHuman Molecular Genetics
researchProduct

In silico pathway analysis in cervical carcinoma reveals potential new targets for treatment

2016

Abstract: An in silico pathway analysis was performed in order to improve current knowledge on the molecular drivers of cervical cancer and detect potential targets for treatment. Three publicly available Affymetrix gene expression data-sets (GSE5787, GSE7803, GSE9750) were retrieved, vouching for a total of 9 cervical cancer cell lines (CCCLs), 39 normal cervical samples, 7 CIN3 samples and 111 cervical cancer samples (CCSs). Predication analysis of microarrays was performed in the Affymetrix sets to identify cervical cancer biomarkers. To select cancer cell-specific genes the CCSs were compared to the CCCLs. Validated genes were submitted to a gene set enrichment analysis (GSEA) and Expre…

0301 basic medicineUterine Cervical NeoplasmMAPK3Uterine Cervical NeoplasmsBioinformaticsHeLa CellMitogen-Activated Protein Kinase0302 clinical medicineTransforming Growth Factor betaMedicineOligonucleotide Array Sequence AnalysisCancerCervical cancerABLCell CycleIn silico pathway analysiCell cycleGene Expression Regulation NeoplasticOncology030220 oncology & carcinogenesisFemaleDNA microarrayMitogen-Activated Protein KinasesTreatment targetResearch PaperHumanin silico pathway analysisMAP Kinase Signaling SystemIn silicoComputational biologytreatment targetsProto-Oncogene Proteins c-myc03 medical and health sciencesCell Line TumorBiomarkers TumorHumansComputer SimulationAmino Acid SequenceBiologyCervical carcinomabusiness.industryOligonucleotide Array Sequence AnalysiGene Expression ProfilingCancerComputational Biologymedicine.diseaseChromatin Assembly and DisassemblyGene expression profiling030104 developmental biologyHuman medicinebusinessHeLa CellsOncotarget
researchProduct

Biological Effect of a Hybrid Anticancer Agent Based on Kinase and Histone Deacetylase Inhibitors on Triple-Negative (MDA-MB231) Breast Cancer Cells

2016

We examined the effects of the histone deacetylase inhibitor (HDACi) suberoylanilide\ud hydroxamic acid (SAHA) combined with the vascular endothelial growth factor receptor-1/2 inhibitor\ud (3Z)-5-hydroxy-3-(1H-pyrrol-2-ylmethylidene)-2,3-dihydro-1H-indol-2-one on MDA-MB-231 breast\ud cancer cells (triple-negative) in the form of both a cocktail of the separate compounds and a chemically\ud synthesized hybrid (N-hydroxy-N'-[(3Z)-2-oxo-3-(1H-pyrrol-2-ylmethylidene)-2,3-dihydro-1H-indol-\ud 5-yl]octanediamide). Comparative flow cytometric and Western blot analyses were performed on\ud cocktail- and hybrid-treated cells to evaluate cell cycle distribution, autophagy/apoptosis modulation,\ud an…

0301 basic medicineVascular Endothelial Growth Factor AIndolesCytotoxicityTriple Negative Breast Neoplasmsbreast cancer; MDA-MB231 cells; histone deacetylase inhibitor; vascular endothelial growth factor receptor-2 inhibitor; cytotoxicity; cell cycle; apoptosis; autophagy; mitochondrial metabolismHydroxamic AcidsCatalysi0302 clinical medicineBreast cancerTumor Cells CulturedCytotoxic T cellSettore BIO/06 - Anatomia Comparata E CitologiaSpectroscopyVorinostatVascular endothelial growth factor receptor-2 inhibitorApoptosis; Autophagy; Breast cancer; Cell cycle; Cytotoxicity; Histone deacetylase inhibitor; MDA-MB231 cells; Mitochondrial metabolism; Vascular endothelial growth factor receptor-2 inhibitor; Catalysis; Molecular Biology; Spectroscopy; Computer Science Applications1707 Computer Vision and Pattern Recognition; Physical and Theoretical Chemistry; Organic Chemistry; Inorganic ChemistryKinaseHistone deacetylase inhibitorapoptosisComputer Science Applications1707 Computer Vision and Pattern RecognitionGeneral MedicineCell cycleFlow CytometryComputer Science ApplicationsCell biologyMDA-MB231 cell030220 oncology & carcinogenesisFemaleQD0241Programmed cell deathmedicine.drug_classCell SurvivalBlotting WesternAntineoplastic AgentsBiologyCell cycleCatalysisArticleInorganic Chemistry03 medical and health sciencesmedicineAutophagyHumansPhysical and Theoretical ChemistryProtein Kinase InhibitorsMolecular BiologyQD0415Histone deacetylase inhibitorAutophagyOrganic ChemistryApoptosiHistone Deacetylase Inhibitors030104 developmental biologyApoptosisMitochondrial metabolismMDA-MB231 cellsHistone deacetylaseInternational Journal of Molecular Sciences; Volume 17; Issue 8; Pages: 1235
researchProduct

GDF11 exhibits tumor suppressive properties in hepatocellular carcinoma cells by restricting clonal expansion and invasion.

2019

Growth differentiation factor 11 (GDF11) has been characterized as a key regulator of differentiation in cells that retain stemness features, despite some controversies in age-related studies. GDF11 has been poorly investigated in cancer, particularly in those with stemness capacity, such as hepatocellular carcinoma (HCC), one of the most aggressive cancers worldwide. Here, we focused on investigating the effects of GDF11 in liver cancer cells. GDF11 treatment significantly reduced proliferation, colony and spheroid formation in HCC cell lines. Consistently, down-regulation of CDK6, cyclin D1, cyclin A, and concomitant upregulation of p27 was observed after 24 h of treatment. Interestingly,…

0301 basic medicine[SDV]Life Sciences [q-bio]Cyclin ACellChick EmbryoChorioallantoic Membrane0302 clinical medicineCell MovementCyclin D1HCCbiologyNeovascularization PathologicCell DifferentiationHep G2 CellsCell cycleCadherinsHuh7 cells3. Good health[SDV] Life Sciences [q-bio]Gene Expression Regulation NeoplasticGrowth Differentiation Factorsmedicine.anatomical_structure030220 oncology & carcinogenesisBone Morphogenetic ProteinsMolecular MedicineLiver cancerCyclin-Dependent Kinase Inhibitor p27Signal Transduction[SDV.CAN]Life Sciences [q-bio]/CancerCyclin ACell cycleHep3B cells03 medical and health sciencesCyclin D1Downregulation and upregulation[SDV.CAN] Life Sciences [q-bio]/CancerAntigens CDCell Line TumorOccludinSpheroids CellularmedicineAnimalsHumansViability assayMolecular BiologyCell Proliferation[SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and GastroenterologyCyclin-Dependent Kinase 6[SDV.MHEP.HEG] Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterology030104 developmental biologyCell cultureGDF11biology.proteinCancer researchCyclin-dependent kinase 6Snail Family Transcription FactorsBiochimica et biophysica acta. Molecular basis of disease
researchProduct