Search results for "Retinoblastoma protein"

showing 10 items of 30 documents

Centrosome amplification induced by hydroxyurea leads to aneuploidy in pRB deficient human and mouse fibroblasts.

2006

Alterations in the number and/or morphology of centrosomes are frequently observed in human tumours. However, it is still debated if a direct link between supernumerary centrosomes and tumorigenesis exists and if centrosome amplification could directly cause aneuploidy. Here, we report that hydroxyurea treatment induced centrosome amplification in both human fibroblasts expressing the HPV16 -E6-E7 oncoproteins, which act principally by targeting p53 and pRB, respectively, and in conditional pRB deficient mouse fibroblasts. Following hydroxyurea removal both normal and p53 deficient human fibroblasts arrested. On the contrary pRB deficient fibroblasts entered the cell cycle generating aneupl…

Cancer ResearchAneuploidyCentrosome amplificationBiologymedicine.disease_causeRetinoblastoma ProteinCell LineMicepRBChromosomal InstabilitymedicineDeficient mouseAnimalsHumansHydroxyureaCINCells CulturedCentrosomeDNA synthesisCell cycleFibroblastsmedicine.diseaseAneuploidyCell biologySettore BIO/18 - GeneticaOncologyCentrosomeAneuploid CellsCarcinogenesisCancer letters
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The effect of 3-aminobenzamide, inhibitor of poly(ADP-ribose) polymerase, on human osteosarcoma cells

2003

This study demonstrates that in human osteosarcoma cells treatment with 3-aminobenzamide (3-AB), a potent inhibitor of poly(ADP-ribose) polymerase (PARP), induces morphological and biochemical features of differentiation, the duration of which depends on whether or not the normal RB gene is expressed. In Saos-2 cells expressing a non-functional Rb protein, 3-AB treatment induced the formation of transient, short dendritic-like protrusions. In RB-transfected-Saos-2 cells (a clone previously generated in our laboratory that shows stable expression of wild-type Rb protein), 3-AB induced marked and prolonged changes with the formation of long dendritic-like protrusions and the appearance of ste…

Cancer ResearchProgrammed cell deathCell typeTime FactorsTranscription GeneticCell SurvivalPoly ADP ribose polymeraseCellular differentiationBlotting WesternApoptosisDNA FragmentationPoly(ADP-ribose) Polymerase InhibitorsBiologyTransfectionPolymerase Chain ReactionRetinoblastoma Proteinchemistry.chemical_compoundCell Line TumorProto-Oncogene ProteinsHumansMicroscopy Phase-ContrastRNA MessengerEnzyme Inhibitorsbcl-2-Associated X ProteinOsteosarcomaLamin Type BCaspase 3Reverse Transcriptase Polymerase Chain ReactionCell DifferentiationDendritesCell cycleAlkaline PhosphataseFlow CytometryMolecular biologyChromatinHyaluronan ReceptorsProto-Oncogene Proteins c-bcl-2OncologychemistryApoptosis3-AminobenzamideCaspasesBenzamides3-aminobenzamide osteosarcoma cells PARP activityAlkaline phosphataseInternational Journal of Oncology
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pRb suppresses camptothecin-induced apoptosis in human osteosarcoma Saos-2 cells by inhibiting c-Jun N-terminal kinase

2001

AbstractThis paper studies the cytotoxic effect induced by the topoisomerase I inhibitor camptothecin in human osteosarcoma Saos-2 cells, which lack p53 and contain a non-functional form of the product of the retinoblastoma gene, pRb. Cytotoxicity induced by camptothecin was dose- and time-dependent; the treatment with 100 nM camptothecin reduced cell viability by 50% at 32 h and by 75% at 72 h of exposure. The cytotoxic effect was caused by apoptosis, as ascertained by morphological evidence, acridine orange-ethidium bromide staining and flow cytometric analysis. Apoptosis was accompanied by both the activation of caspase-3 and the fragmentation of poly(ADP-ribose) polymerase. Treatment wi…

Time FactorsCell SurvivalProto-Oncogene Proteins c-junBlotting WesternBiophysicsApoptosisBiologyTransfectionRetinoblastoma ProteinBiochemistryStructural BiologyTumor Cells CulturedpRb JNK topoisomerase I inhibitors osteosarcomaGeneticsmedicineHumansCytotoxic T cellViability assayPhosphorylationFragmentation (cell biology)neoplasmsMolecular BiologySaos-2 cellsc-Jun N-terminal kinaseCell SizeDose-Response Relationship DrugCaspase 3Cell growthCell Cyclec-junJNK Mitogen-Activated Protein KinasesHydrogen PeroxideCell BiologyFlow CytometryGlutathioneMolecular biologyEnzyme ActivationOxidative StresspRbDNA Topoisomerases Type IApoptosisCaspasesCamptothecinMitogen-Activated Protein KinasesPoly(ADP-ribose) PolymerasesTopoisomerase I InhibitorsCamptothecinmedicine.drugFEBS Letters
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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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2,3,7,8-Tetrachlorodibenzo-p-dioxin-Dependent Release from Contact Inhibition in WB-F344 Cells: Involvement of Cyclin A

2002

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is the most potent tumor promoter ever tested in rodents. Although it is known that most of TCDD actions are mediated by binding to the aryl hydrocarbon receptor (AhR), the mechanisms leading to tumor promotion still remain to be elucidated. Loss of contact inhibition is one characteristic hallmark in tumorigenesis. In rat liver epithelial WB-F344 cells, TCDD induces a release from contact inhibition, which is manifested by a twofold increase in cell number when TCDD (1 nM for 48 h) is added to confluent cells in the presence of serum, but not when given to exponentially growing or subconfluent, serum-deprived WB-F344 cells. Loss of G1 arrest was a…

Pharmacologyendocrine systemmedicine.medical_specialtybiologyCyclin DCyclin-dependent kinase 2Cyclin ARetinoblastoma proteinContact inhibitionToxicologyMolecular biologystomatognathic diseasesEndocrinologyCyclin D2Cyclin-dependent kinaseInternal medicinebiology.proteinmedicineheterocyclic compoundsCyclinToxicology and Applied Pharmacology
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Suppressor activity of anergic T cells induced by IL-10-treated human dendritic cells: association with IL-2- and CTLA-4-dependent G1 arrest of the c…

2003

We have previously shown that human IL-10-treated dendritic cells (DC) induce an antigen-specific anergy in CD4+ T lymphocytes. These anergic T cells are characterized by an inhibited proliferation, a reduced production of IL-2, and additionally display antigen-specific suppressor activity. In this study we investigated the mechanisms underlying the anergic state and regulatory function of these T cells. We did not observe enhanced rates of programmed cell death of anergic CD4+ suppressor T cells compared to T cells stimulated with mature DC. Cell cycle analysis by DNA staining and Western blot experiments revealed an arrest of anergic CD4+ T suppressor cells in the G1 phase. High levels of…

ImmunoconjugatesRegulatory T cellT-LymphocytesImmunologyApoptosisCell Cycle ProteinsAbataceptCyclin-dependent kinaseAntigens CDmedicineImmunology and AllergyHumansCTLA-4 AntigenIL-2 receptorClonal AnergybiologyTumor Suppressor ProteinsRetinoblastoma proteinDendritic cellDendritic CellsCell cycleAntigens DifferentiationCell biologyInterleukin-10Interleukin 10medicine.anatomical_structurebiology.proteinInterleukin-2CDK inhibitorCell DivisionCyclin-Dependent Kinase Inhibitor p27European journal of immunology
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RNAi mediated acute depletion of Retinoblastoma protein (pRb) promotes aneuploidy in human primary cells via micronuclei formation

2009

BACKGROUND: Changes in chromosome number or structure as well as supernumerary centrosomes and multipolar mitoses are commonly observed in human tumors. Thus, centrosome amplification and mitotic checkpoint dysfunctions are believed possible causes of chromosomal instability. The Retinoblastoma tumor suppressor (RB) participates in the regulation of synchrony between DNA synthesis and centrosome duplication and it is involved in transcription regulation of some mitotic genes. Primary human fibroblasts were transfected transiently with short interfering RNA (siRNA) specific for human pRb to investigate the effects of pRb acute loss on chromosomal stability. RESULTS: Acutely pRb-depleted fibr…

Small interfering RNAMitosisCell Cycle ProteinsProtein Serine-Threonine KinasesRetinoblastoma ProteinAurora KinasesRNA interferenceChromosomal InstabilityProto-Oncogene ProteinsChromosome instabilitymedicineHumansCentrosome duplicationRNA Small Interferinglcsh:QH573-671MitosisCells CulturedCell NucleusCentrosomebiologylcsh:CytologyRetinoblastomaRetinoblastoma proteinCell BiologyFibroblastsAneuploidymedicine.diseaseCell biologyCentrosomeRNAi Aneuploidy pRBRb anauploidybiology.proteinRNA Interferencebiological phenomena cell phenomena and immunityResearch ArticleBMC Cell Biology
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2-Hydroxyoleate, a nontoxic membrane binding anticancer drug, induces glioma cell differentiation and autophagy

2012

Despite recent advances in the development of new cancer therapies, the treatment options for glioma remain limited, and the survival rate of patients has changed little over the past three decades. Here, we show that 2-hydroxyoleic acid (2OHOA) induces differentiation and autophagy of human glioma cells. Compared to the current reference drug for this condition, temozolomide (TMZ), 2OHOA combated glioma more efficiently and, unlike TMZ, tumor relapse was not observed following 2OHOA treatment. The novel mechanism of action of 2OHOA is associated with important changes in membrane-lipid composition, primarily a recovery of sphingomyelin (SM) levels, which is markedly low in glioma cells bef…

MaleProgrammed cell deathTime FactorsCell SurvivalMAP Kinase Signaling SystemCellular differentiationMice NudeAntineoplastic AgentsOleic AcidsBiologyglioma biomarkerfatty acidsMembrane LipidsMicePhosphatidylinositol 3-Kinases2-Hydroxyoleic AcidGliomaCell Line TumormedicineAutophagyTemozolomideAnimalsHumansPI3K/AKT/mTOR pathwayCell ProliferationMultidisciplinaryTemozolomideMicroscopy ConfocalDose-Response Relationship DrugCell growthCell MembraneRetinoblastoma proteinCell DifferentiationGliomaBiological Sciencesmedicine.diseaseXenograft Model Antitumor AssaysCell biologyDacarbazineProtein TransportCancer researchbiology.proteinras Proteinssphingomyelin synthaseProto-Oncogene Proteins c-aktcancer drug targetmedicine.drug
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Mechanisms of environmental chemicals that enable the cancer hallmark of evasion of growth suppression

2015

As part of the Halifax Project, this review brings attention to the potential effects of environmental chemicals on important molecular and cellular regulators of the cancer hallmark of evading growth suppression. Specifically, we review the mechanisms by which cancer cells escape the growth-inhibitory signals of p53, retinoblastoma protein, transforming growth factor-beta, gap junctions and contact inhibition. We discuss the effects of selected environmental chemicals on these mechanisms of growth inhibition and cross-reference the effects of these chemicals in other classical cancer hallmarks.

Cancer ResearchReviewHazardous Substanceschemistry.chemical_compoundNeoplasmsAnimalsHumansMedicinebiologyAnimalbusiness.industryMedicine (all)Retinoblastoma proteinContact inhibitionCancerEnvironmental ExposureGeneral MedicineEnvironmental exposureEvasion (ethics)medicine.diseaseCell biologychemistryHazardous SubstanceImmunologyCancer cellbiology.proteinNeoplasmSignal transductionGrowth inhibitionbusinessHumanSignal TransductionCarcinogenesis
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Synthesis and antiproliferative activity of 3-amino-N-phenyl-1H-indazole-1-carboxamides

2007

Abstract A series of new 3-amino-N-phenyl-1H-indazole-1-carboxamides 10 have been prepared from commercially available phenyl isocyanate precursors 8 and 3-aminoindazole 9. Some of the synthesized compounds were evaluated for their in vitro antineoplastic activity against 60 human cell lines derived from seven clinically isolated cancer types (lung, colon, melanoma, renal, ovarian, brain, and leukemia) according to the NCI standard protocol. The test results indicated that 3-amino-1H-indazole-1-carboxamides 10 were endowed with an interesting antiproliferative activity. The most active compounds of this series, 10d,e, were able to inhibit cell growth of many neoplastic cell lines at concent…

IndazolesAntineoplastic AgentsCrystallography X-RayRetinoblastoma Proteinchemistry.chemical_compoundStructure-Activity RelationshipCell Line TumorNeoplasmsDrug DiscoverymedicineHumansCell ProliferationG0-G1 arrestPharmacologyIndazoleMolecular StructureChemistryCell growthMelanomaOrganic ChemistryCell CycleCancer1H-Indazole-1-carboxamides; Crystallographic study; G0-G1 arrest; pRb1H-Indazole-1-carboxamideGeneral MedicineCell cyclemedicine.diseaseAmidesSettore CHIM/08 - Chimica FarmaceuticaIn vitroCrystallographyc studyLeukemiapRbBiochemistryNeoplastic cell
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