Search results for "Cell Cycle Protein"

showing 10 items of 131 documents

Differentiative pathway activated by 3-aminobenzamide, an inhibitor of PARP, in human osteosarcoma MG-63 cells

2004

AbstractThis study describes the molecular mechanism by which treatment with 3-AB, a potent inhibitor of PARP, allows human osteosarcoma MG-63 cells to restrict growth and enter differentiation. Our findings show that in MG-63 cells, aberrant gene expression keeps Rb protein constitutively inactivated through hyperphosphorylation and this promotes uncontrolled proliferation of the cells. After 3-AB-treatment, the poly(ADP-ribosyl)ation of nuclear proteins markedly decreases and this results in an increase in both the hypophosphorylated active form of Rb and pRb/E2F complexes. These effects are accompanied by G1 arrest, downregulation of gene products required for proliferation (cyclin D1, β…

Blotting WesternBiophysicsHyperphosphorylationCell Cycle ProteinsPoly(ADP-ribose) Polymerase InhibitorsCell cycleRetinoblastoma ProteinBiochemistryPARPRb proteinCyclin D1Downregulation and upregulationStructural BiologyCell Line TumorGene expressionGeneticsHumansImmunoprecipitationOsteopontinEnzyme InhibitorsPhosphorylationE2FMolecular BiologyDNA PrimersAdenosine Diphosphate RiboseOsteosarcomaBase SequencebiologyReverse Transcriptase Polymerase Chain ReactionG1 PhaseCell DifferentiationCell BiologyCell cycleFlow Cytometry3-ABE2F Transcription FactorsChromatinDNA-Binding ProteinsGene Expression RegulationDifferentiationBenzamidesbiology.proteinCancer researchTranscription FactorsFEBS Letters
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The transcriptional programme of contact-inhibition.

2010

Proliferation of non-transformed cells is regulated by cell-cell contacts, which are referred to as contact-inhibition. Vice versa, transformed cells are characterised by a loss of contact-inhibition. Despite its generally accepted importance for cell-cycle control, little is known about the intracellular signalling pathways involved in contact-inhibition. Unravelling the molecular mechanisms of contact-inhibition and its loss during tumourigenesis will be an important step towards the identification of novel target genes in tumour diagnosis and treatment. To better understand the underlying molecular mechanisms we identified the transcriptional programme of contact-inhibition in NIH3T3 fib…

Blotting WesternClone (cell biology)Cell Cycle ProteinsBiologyBiochemistryMiceComplementary DNATranscriptional regulationAnimalsMolecular BiologyGeneRegulator geneOligonucleotide Array Sequence AnalysisContact InhibitionReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingCell CycleContact inhibitionCell BiologyFibroblastsFlow CytometryMolecular biologyGene expression profilingNIH 3T3 CellsDNA microarraySignal TransductionJournal of cellular biochemistry
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MYCN sensitizes human neuroblastoma to apoptosis by HIPK2 activation through a DNA damage response.

2010

Abstract MYCN amplification occurs in approximately 20% of human neuroblastomas and is associated with early tumor progression and poor outcome, despite intensive multimodal treatment. However, MYCN overexpression also sensitizes neuroblastoma cells to apoptosis. Thus, uncovering the molecular mechanisms linking MYCN to apoptosis might contribute to designing more efficient therapies for MYCN-amplified tumors. Here we show that MYCN-dependent sensitization to apoptosis requires activation of p53 and its phosphorylation at serine 46. The p53S46 kinase HIPK2 accumulates on MYCN expression, and its depletion by RNA interference impairs p53S46 phosphorylation and apoptosis. Remarkably, MYCN ind…

Cancer ResearchApoptosisCell Cycle ProteinsAtaxia Telangiectasia Mutated ProteinsProtein-Serine-Threonine KinaseAtaxia Telangiectasia Mutated ProteinNeuroblastomaCell Cycle ProteinSerinePhosphorylationNuclear ProteinOncogene Proteinseducation.field_of_studyN-Myc Proto-Oncogene ProteinAntibiotics AntineoplasticKinaseOncogene ProteinNuclear ProteinsDNA-Binding ProteinsOncologyPhosphorylationRNA InterferenceHumanDNA damageDNA-Binding ProteinPopulationBlotting WesternBiologyProtein Serine-Threonine KinasesN-Myc Proto-Oncogene ProteinBleomycinNeuroblastomaCell Line TumormedicineHumanseducationneoplasmsMolecular BiologyTumor Suppressor ProteinTumor Suppressor ProteinsApoptosimedicine.diseaseTumor progressionApoptosisMutationCancer researchTumor Suppressor Protein p53Carrier ProteinCarrier ProteinsDNA DamageMolecular cancer research : MCR
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The novel NF-κB inhibitor DHMEQ synergizes with celecoxib to exert antitumor effects on human liver cancer cells by a ROS-dependent mechanism

2012

In a previous work of ours dehydroxymethyl-epoxyquinomicin (DHMEQ), an inhibitor of NF-κB, was shown to induce apoptosis through Reactive Oxygen Species (ROS) production in hepatoma cells. The present study demonstrated that DHMEQ cooperates with Celecoxib (CLX) to decrease NF-κB DNA binding and to inhibit cell growth and proliferation more effectively than treatment with these single agents alone in the hepatoma cell lines HA22T/VGH and Huh-6. ROS production induced by the DHMEQ-CLX combination in turn generated the expression of genes involved in endoplasmic reticulum (ER) stress and silencing TRB3 mRNA significantly decreased DHMEQ-CLX-induced cell growth inhibition. Moreover, the DHMEQ-…

Cancer ResearchCarcinoma HepatocellularAntineoplastic AgentsApoptosisCell Cycle ProteinsProtein Serine-Threonine KinasesBiologyDHMEQ Celecoxib NF-jB CD95/CD95L Liver cancer cellsCell Line TumorSurvivinHumansGene silencingfas ReceptorProtein kinase BCell ProliferationSulfonamidesGene knockdownCyclooxygenase 2 InhibitorsCyclohexanonesCell growthEndoplasmic reticulumLiver NeoplasmsNF-kappa BDrug SynergismEndoplasmic Reticulum StressMolecular biologyAcetylcysteineRepressor ProteinsOncologyCelecoxibCell cultureApoptosisBenzamidesCancer researchPyrazolesPoly(ADP-ribose) PolymerasesReactive Oxygen SpeciesCancer Letters
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Differences in the mechanisms of growth control in contact-inhibited and serum-deprived human fibroblasts

1997

In the present work we studied mechanisms of growth control in contact-inhibited and serum-deprived human diploid fibroblasts. The observation that the effects on [3H]thymidine incorporation and reduction of retinoblastoma gene product-phosphorylation were additive when contact-inhibition and serum-deprivation were combined led us to the conclusion that the underlying mechanisms might be different. Both contact-inhibition and serum-deprivation led to a strong decrease of cdk4-kinase-activity and cdk2-phosphorylation at Thr 160, while the total amounts of cdk4 and cdk2 remained constant. In contact-inhibited cells, we revealed a strong protein accumulation of the cdk2-inhibitor p27 and a sli…

Cancer ResearchCell Cycle ProteinsProtein Serine-Threonine KinasesRetinoblastoma ProteinCulture Media Serum-FreeS PhaseCyclin D1CyclinsProto-Oncogene ProteinsCDC2-CDC28 KinasesGeneticsmedicineHumansCyclin D1Cyclin D3PhosphorylationCyclin D3FibroblastMolecular BiologyCyclin-Dependent Kinase Inhibitor p16CyclinbiologyCell growthTumor Suppressor ProteinsCyclin-Dependent Kinase 2Cyclin-dependent kinase 2G1 PhaseCyclin-Dependent Kinase 4FibroblastsDiploidyCyclin-Dependent KinasesCulture MediaCell biologymedicine.anatomical_structureCell culturebiology.proteinbiological phenomena cell phenomena and immunitySignal transductionMicrotubule-Associated ProteinsCell DivisionCyclin-Dependent Kinase Inhibitor p27Oncogene
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Bioactivity of well-defined green tea extracts in multicellular tumor spheroids.

2002

The effect of green tea extracts (GTE) of a reproducible, well-defined composition on cellular viability, proliferation, and antioxidant defense was investigated in multicellular spheroids derived from WiDr human colon adenocarcinoma cells. The maximum GTE concentration investigated, i.e. 100 micro g GTE/ml, was equivalent to the plasma concentration commonly measured in humans drinking 6-10 cups of green tea per day. This GTE concentration lead to a substantial retardation of spheroid volume growth with diameters reaching only half the size of untreated aggregates. Flow cytometric analysis and immunocytochemistry showed an enhanced accumulation of cells in G2/M and in the non-proliferating…

Cancer ResearchCellular pathologyPathologymedicine.medical_specialtyCellCell Cycle ProteinsBiologyAdenocarcinomachemistry.chemical_compoundSpheroids CellularmedicineCell AdhesionTumor Cells CulturedHumansChromatography High Pressure LiquidTumor Stem Cell AssayTeaCell growthPlant ExtractsCell CycleSpheroidGlutathioneCadherinsMolecular biologyGlutathionemedicine.anatomical_structureKi-67 AntigenOncologychemistryCell cultureApoptosisembryonic structuresToxicityColonic NeoplasmsFemaleInternational journal of oncology
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Effects of resveratrol analogs on cell cycle progression, cell cycle associated proteins and 5fluoro-uracil sensitivity in human derived colon cancer…

2009

International audience; Epidemiological studies suggested that trans-resveratrol, a wine grape component, could prevent malignant tumor development. This compound also demonstrated cytostatic and cytotoxic effects on tumor cells in vitro. To obtain trans-resveratrol derivatives with a better cellular uptake and enhanced antiproliferative effects, we synthesized a triacetate derivative as well as an oligomer, epsilon-viniferin and its acetylated form, epsilon-viniferin penta-acetate. We also obtained vineatrol, a wine grape shoot extract that associates several polyphenols that may act synergistically, including trans-resveratrol and epsilon-viniferin. We show here that resveratrol triacetat…

Cancer ResearchCyclin AFluorescent Antibody TechniqueCell Cycle ProteinsMESH: Cell CycleMESH: Flow CytometryMESH : Blotting WesternResveratrolmedicine.disease_causeWine grapeMESH: Drug SynergismImmunoenzyme Techniqueschemistry.chemical_compoundMESH: PhenolsMESH : Cell Cycle ProteinsMESH : Tumor Cells CulturedMESH: StilbenesStilbenesTumor Cells CulturedMESH : Cell ProliferationMESH: Fluorescent Antibody TechniqueMESH: Antimetabolites AntineoplasticbiologyKinaseMESH : Antimetabolites AntineoplasticCell Cyclefood and beveragesDrug SynergismCell cycleFlow CytometryMESH : Colonic NeoplasmsOncologyBiochemistryColonic NeoplasmsMESH : FluorouracilFluorouracilMESH : PhenolsAntimetabolites AntineoplasticMESH : Drug SynergismMESH : Flow CytometryBlotting WesternMESH : ImmunoprecipitationMESH : StilbenesMESH: Cell Cycle ProteinsPhenolsMESH : Immunoenzyme TechniquesMESH: Cell ProliferationMESH : Cell Cycle[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologymedicineHumansImmunoprecipitationMESH: Blotting Western[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: Tumor Cells CulturedKinase activityMESH: Immunoenzyme Techniques[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyBenzofuransCell ProliferationMESH: Colonic NeoplasmsMESH: HumansMESH : BenzofuransMESH: ImmunoprecipitationMESH : HumansMESH: BenzofuransMESH : Fluorescent Antibody TechniquechemistryResveratrolCell culturebiology.proteinCarcinogenesisMESH: Fluorouracil
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Artesunate induces oxidative DNA damage, sustained DNA double-strand breaks, and the ATM/ATR damage response in cancer cells.

2011

Abstract Artesunate, the active agent from Artemisia annua L. used in the traditional Chinese medicine, is being applied as a first-line drug for malaria treatment, and trials are ongoing that include this drug in cancer therapy. Despite increasing interest in its therapeutic application, the mode of cell killing provoked by artesunate in human cells is unknown. Here, we show that artesunate is a powerful inducer of oxidative DNA damage, giving rise to formamidopyrimidine DNA glycosylase–sensitive sites and the formation of 8-oxoguanine and 1,N6-ethenoadenine. Oxidative DNA damage was induced in LN-229 human glioblastoma cells dose dependently and was paralleled by cell death executed by ap…

Cancer ResearchProgrammed cell deathDNA RepairRAD51Drug Evaluation PreclinicalArtesunateApoptosisCell Cycle ProteinsAtaxia Telangiectasia Mutated ProteinsBiologyProtein Serine-Threonine KinasesModels Biologicalchemistry.chemical_compoundNeoplasmsTumor Cells CulturedHumansDNA Breaks Double-StrandedTumor Suppressor ProteinsMolecular biologyAntineoplastic Agents PhytogenicArtemisininsUp-RegulationNon-homologous end joiningDNA-Binding ProteinsOxidative StressCell killingOncologychemistryArtesunateApoptosisCancer cellHomologous recombinationDNA DamageMolecular cancer therapeutics
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GADD45α is highly expressed in pancreatic ductal adenocarcinoma cells and required for tumor cell viability

2005

Pancreatic ductal adenocarcinoma is one of the most common causes of cancer death in the western civilization. Recently, NF-kappaB has been shown to be activated in pancreatic ductal adenocarcinoma through constitutive activation of IkappaB kinase (IKK). Inhibition of NF-kappaB by a super-inhibitor of NF-kappaB--delta-N-IkappaBalpha--resulted in impaired proliferation and induction of apoptosis, suggesting an important role of NF-kappaB in pancreatic tumorigenesis. Downstream target genes of IkappaBalpha have not been elucidated in pancreatic ductal adenocarcinoma in detail. Using expression profiling by cDNA array analysis of pancreatic ductal adenocarcinoma cell lines stably transfected w…

Cancer Researchmedicine.medical_specialtyPancreatic diseaseCell SurvivalDown-RegulationCell Cycle ProteinsIκB kinaseAdenocarcinomaBiologymedicine.disease_causeDownregulation and upregulationPancreatic cancerInternal medicinemedicineHumansCell ProliferationCell growthGene Expression ProfilingNF-kappa BNuclear Proteinsmedicine.diseaseI-kappa B KinasePancreatic NeoplasmsEndocrinologyOncologyApoptosisCancer researchRNA InterferenceCA19-9CarcinogenesisCarcinoma Pancreatic DuctalInternational Journal of Cancer
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Spatial regulation of the Start repressor Whi5

2009

The Saccharomyces cerevisiae Start repressor Whi5, the functional analogue of mammalian pRB, shuttles between the nucleus and the cytoplasm throughout the cell cycle: enters into the nucleus at the end of mitosis and remains nuclear until Start. We studied the mechanisms involved in this spatial regulation. The nuclear import depends on the beta-karyopherins of the classical import pathway Kap95 and Cse1. Whi5 contains a monopartite and a bipartite classical NLS localized in its N-terminal region which are functionally redundant. A fragment of Whi5 containing these NLSs is able to constitutively accumulate a GFP(4) protein inside the nucleus throughout the cell cycle, which suggests that th…

Cdc14Cell BiologyBiologyCell biologyCell nucleusmedicine.anatomical_structureBiochemistryCytoplasmmedicineNuclear transportNuclear proteinNuclear export signalCell Cycle ProteinMolecular BiologyMitosisDevelopmental BiologyCell Cycle
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