Search results for "pRB"

showing 10 items of 22 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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Sodium butyrate induces apoptosis in human hepatoma cells by a mitochondria/caspase pathway, associated with degradation of beta-catenin, pRb and Bcl…

2004

Butyrate can promote programmed cell death in a number of tumour cells in vitro. This paper provides evidence that butyrate induces apoptosis in human hepatoma HuH-6 and HepG2 cells but is ineffective in Chang liver cells, an immortalised non-tumour cell line. In both HuH-6 and HepG2 cells, apoptosis appeared after a lag period of approximately 16 h and increased rapidly during the second day of treatment. In particular, the effect was stronger in HuH-6 cells, which were, therefore, chosen for ascertaining the mechanism of butyrate action. In HuH-6 cells, beta-catenin seemed to exert an important protective role against apoptosis, since pretreatment with beta-catenin antisense ODN reduced t…

Cancer ResearchProgrammed cell deathbeta-CateninCarcinoma HepatocellularBlotting Westernbcl-X ProteinCaspase 3Bcl-xLApoptosisButyrateCell LineMembrane Potentialschemistry.chemical_compoundSettore BIO/10 - BiochimicaCyclin DCyclinsCyclin EHumansCaspasebeta CateninbiologyReverse Transcriptase Polymerase Chain ReactionCytochrome cLiver NeoplasmsSodium butyrateMolecular biologyButyratesCytoskeletal ProteinspRbOncologychemistryProto-Oncogene Proteins c-bcl-2ApoptosisCaspasesbiology.proteinTrans-ActivatorsPoly(ADP-ribose) PolymerasesEuropean journal of cancer (Oxford, England : 1990)
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pRb2/p130-E2F4/5-HDAC1-SUV39H1-p300 and pRb2/p130-E2F4/5-HDAC1-SUV39H1-DNMT1 multimolecular complexes mediate the transcription of estrogen receptor-…

2003

The estrogen receptor-alpha (ER) plays a crucial role in normal breast development and is also linked to development and progression of mammary carcinoma. The transcriptional repression of ER-alpha gene in breast cancer is an area of active investigation with potential clinical significance. However, the molecular mechanisms that regulate the ER-alpha gene expression are not fully understood. Here we show a new molecular mechanism of ER-alpha gene inactivation mediated by pRb2/p130 in ER-negative breast cancer cells. We investigated in vivo occupancy of ER-alpha promoter by pRb2/p130-E2F4/5-HDAC1-SUV39 H1-p300 and pRb2/p130-E2F4/5-HDAC1-SUV39H1-DNMT1 complexes, and provided a link between p…

Cancer ResearchTranscription GeneticEstrogen receptorHistone Deacetylase 1HistonesTumor Cells CulturedDNA (Cytosine-5-)-MethyltransferasesReceptorPromoter Regions GeneticE2F4Nuclear ProteinsAcetylationChromatinDNA-Binding ProteinsGene Expression Regulation NeoplasticReceptors Estrogenembryonic structuresDNA methylationFemalepRb2/p130; chromatin-modifying enzymes; estrogen receptor-alpha; breast carcinomabiological phenomena cell phenomena and immunityDNA (Cytosine-5-)-Methyltransferase 1medicine.medical_specialtyanimal structuresmedicine.drug_classMacromolecular SubstancesBreast NeoplasmsE2F4 Transcription FactorBiologyHistone DeacetylasesBreast cancerInternal medicineGeneticsmedicineEstrogen Receptor betaHumansMolecular BiologyEstrogen receptor betaE2F5 Transcription FactorRetinoblastoma-Like Protein p130Estrogen Receptor alphaProteinsMethyltransferasesDNA Methylationmedicine.diseasePhosphoproteinsRepressor Proteinsenzymes and coenzymes (carbohydrates)EndocrinologyEstrogenCancer researchTrans-ActivatorsEstrogen receptor alphaTranscription FactorsOncogene
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Functional Inactivation of pRB Results in Aneuploid Mammalian Cells After Release From a Mitotic Block

2002

AbstractThe widespread chromosome instability observed in tumors and in early stage carcinomas suggests that aneuploidy could be a prerequisite for cellular transformation and tumor initiation. Defects in tumor suppressers and genes that are part of mitotic checkpoints are likely candidates for the aneuploid phenotype. By using flow cytometric, cytogenetic, immunocytochemistry techniques we investigated whether pRB deficiency could drive perpetual aneuploidy in normal human and mouse fibroblasts after mitotic checkpoint challenge by microtubule-destabilizing drugs. Both mouse and human pRB-deficient primary fibroblasts resulted, upon release from a mitotic block, in proliferating aneuploid …

DNA ReplicationCancer ResearchBrief ArticleClone (cell biology)MitosisAneuploidyCre recombinaseSpindle Apparatuslcsh:RC254-282Retinoblastoma ProteinColony-Forming Units AssayMicechemistry.chemical_compoundChromosome instabilitymedicineAnimalsHumanscentrosomesCINGenes RetinoblastomaMitosisCells CulturedIn Situ Hybridization FluorescenceCentrosomeCell cycle controlbiologyColcemidChromosome FragilityCell CycleGINDemecolcineRetinoblastoma proteinAneuploidy; Cell cycle control; Centrosomes; CIN; PRB;FibroblastsCell cyclelcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensAneuploidyFlow Cytometrymedicine.diseaseAntineoplastic Agents PhytogenicCell biologyCell Transformation NeoplasticPRBMicroscopy Fluorescencechemistrybiology.proteinFemaleNeoplasia
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CENPA overexpression promotes genome instability in pRb-depleted human cells

2009

Abstract Background Aneuploidy is a hallmark of most human cancers that arises as a consequence of chromosomal instability and it is frequently associated with centrosome amplification. Functional inactivation of the Retinoblastoma protein (pRb) has been indicated as a cause promoting chromosomal instability as well centrosome amplification. However, the underlying molecular mechanism still remains to be clarified. Results Here we show that pRb depletion both in wild type and p53 knockout HCT116 cells was associated with the presence of multipolar spindles, anaphase bridges, lagging chromosomes and micronuclei harbouring whole chromosomes. In addition aneuploidy caused by pRb acute loss was…

Genome instabilityCancer ResearchChromosomal Proteins Non-HistoneBlotting WesternBiologyAutoantigensRetinoblastoma Proteinlcsh:RC254-282Genomic InstabilityRNA interferenceChromosome instabilityCentromere Protein ACell Line TumorHumansRNA Processing Post-TranscriptionalDNA PrimersCENPABase SequenceReverse Transcriptase Polymerase Chain ReactionResearchRetinoblastoma proteincentromere protein aneuploidy pRBlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensMolecular biologyCell biologySettore BIO/18 - GeneticaSpindle checkpointOncologyMicroscopy FluorescenceCentrosomebiology.proteinMolecular MedicineRNA Interferencebiological phenomena cell phenomena and immunityCentromere Protein AMolecular Cancer
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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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Synthesis of substituted 3-amino-N-phenyl-1H-indazole-1-carboxamides endowed with antiproliferative activity

2010

Abstract Several new N-phenyl-1H-indazole-1-carboxamides 1c–h and 4l,m were prepared by reacting phenyl isocyanate derivatives 3a,b with 3-amino-1H-indazole derivatives 2c,e,g or 1H-indazole 2l respectively. Chemical transformations of compounds 1a,b and 1g,h gave 3-acetamido-N-phenyl-1H-indazole-1-carboxamide derivatives 5a,b, and 3,5-diamino-N-phenyl-1H-indazole-1-carboxamide derivatives 4i, j respectively. Finally, 3,5-diacetamido-N-phenyl-1H-indazole-1-carboxamide derivatives 6a,b were prepared by acetylation of 4i, j. Some of synthesized compounds were evaluated for their in vitro antiproliferative activity against the full NCI tumor cell lines panel derived from nine clinically isolat…

IndazolesStereochemistryCellAntineoplastic AgentsRetinoblastoma Proteinchemistry.chemical_compoundCell Line TumorDrug DiscoveryG0–G1 arrestmedicineHumansCell ProliferationPharmacologyIndazoleCell growth3-amino-N-phenyl-1H-indazole-1-carboxamideMelanomaCell CycleOrganic ChemistryAntiproliferative agentsCancerGeneral Medicinemedicine.diseaseSettore CHIM/08 - Chimica FarmaceuticaIn vitropRbmedicine.anatomical_structurechemistryAcetylationK562 cellsEuropean Journal of Medicinal Chemistry
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Natriuretic peptide system expression in murine and human submandibular salivary glands: a study of the spatial localisation of ANB, BNP, CNP and the…

2019

AbstractThe natriuretic peptide (NP) system comprises of three ligands, the Atrial Natriuretic Peptide (ANP), Brain Natriuretic peptide (BNP) and C-type Natriuretic peptide (CNP), and three natriuretic peptide receptors, NPRA, NPRB and NPRC. Here we present a comprehensive study of the natriuretic peptide system in healthy murine and human submandibular salivary glands (SMGs). We show CNP is the dominant NP in mouse and human SMG and is expressed together with NP receptors in ducts, autonomic nerves and the microvasculature of the gland, suggesting CNP autocrine signalling may take place in some of these glandular structures. These data suggest the NP system may control salivary gland funct…

MaleSettore BIO/17 - Istologia0301 basic medicinemedicine.medical_specialtyHistologyReceptors PeptidePhysiologymedicine.drug_classAtrial natriuretic peptide ANPNatriuretic peptide receptor B NPRBMice03 medical and health sciences0302 clinical medicineAtrial natriuretic peptideInternal medicineNatriuretic Peptide BrainmedicineNatriuretic peptideAnimalsHumansAutonomic nervous systemB-type natriuretic peptide BNPNatriuretic peptide receptor C NPRCAutocrine signallingReceptorSalivary glandSubmandibular glandSalivary glandC-type natriuretic peptide CNPChemistryNatriuretic Peptide C-TypeCell BiologyGeneral MedicineNatriuretic peptide receptor A NPRABrain natriuretic peptideSubmandibular glandNeoplasm Proteins030104 developmental biologymedicine.anatomical_structureEndocrinologyOral squamous cell carcinoma030220 oncology & carcinogenesisCarcinoma Squamous CellFemaleMouth NeoplasmsAtrial Natriuretic FactorHomeostasisJournal of Molecular Histology
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Synthesis and antiproliferative activity of new derivatives containing the polycyclic system 5,7:7,13-dimethanopyrazolo[3,4-b]pyrazolo[3’,4’:2,3]azep…

2013

The reaction under reflux between 1-phenyl-3-R-5-methylaminopyrazoles and 2,5-hexanedione lead to 5,7:7,13-dimethanopyrazolo[3,4-b]pyrazolo[3′,4′:2,3]azepino[4,5-f]azocine derivatives 3b–g. These unusual molecules show the structural complexity of many biologically active natural products and are endowed with the chemical diversity that is required in drug discovery. The compounds 3b,e were reduced by hydrogen in the presence of Palladium on activated charcoal to give the dihydro derivatives 5b,e. Compounds 3b–f and 5b,e were selected by the NCI to evaluate their in vitro antiproliferative activity against 60 human cell lines derived from nine clinically isolated cancer types (leukaemia, lu…

Models MolecularStereochemistryAntineoplastic AgentsHL-60 CellsHeterocyclic Compounds 4 or More RingsDephosphorylationchemistry.chemical_compoundStructure-Activity RelationshipCell Line TumorSettore BIO/10 - BiochimicaDrug DiscoverymedicineMoleculeHumansAzocinePolycyclic CompoundsCell ProliferationPharmacologyDose-Response Relationship DrugMolecular StructureDrug discoveryOrganic ChemistryCell CycleCancerBiological activityGeneral MedicineCell cyclemedicine.diseaseSettore CHIM/08 - Chimica FarmaceuticaIn vitrochemistryMCF-7 Cells57:713-dimethanopyrazolo[34-b]pyrazolo[3’4’:23]azepino[45-f]azocine derivatives antiproliferative activity G0-G1 arrest pRbDrug Screening Assays AntitumorK562 Cells
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Adenoviral RB2/p130 gene transfer inhibits smooth muscle cell proliferation and prevents restenosis after angioplasty.

1999

Abstract —Smooth muscle cell (SMC) proliferation that results in neointima formation is implicated in the pathogenesis of atherosclerotic plaques and accounts for the high rates of restenosis that occur after percutaneous transluminal coronary angioplasty, a widespread treatment for coronary artery disease. Endothelial lesions trigger intense proliferative signals to the SMCs of the subintima, stimulating their reentry into the cell cycle from a resting G 0 state, resulting in neointima formation and vascular occlusion. Cellular proliferation is negatively controlled by growth-regulatory or tumor-suppressor genes, or both, such as the retinoblastoma gene family members ( RB/p105, p107, RB2…

NeointimaTranscriptional Activationmedicine.medical_specialtyPhysiologyadenovirus; cell cycle; gene therapy; p130; prb2; restenosisCellGenetic VectorsCell Cycle ProteinsPulmonary ArteryMuscle Smooth VascularAdenoviridaeCatheterizationPathogenesisRestenosisRecurrencemedicineAnimalsCarotid StenosisAngioplasty Balloon CoronaryGenes RetinoblastomaCells CulturedNeointimal hyperplasiaWound HealingRetinoblastoma-Like Protein p130business.industryCell growthGenetic transferCell CycleProteinsGenetic TherapyCell cyclemedicine.diseasePhosphoproteinsSurgeryE2F Transcription FactorsRatsDNA-Binding Proteinsmedicine.anatomical_structureCancer researchCardiology and Cardiovascular MedicinebusinessCarotid Artery InjuriesCarrier ProteinsTunica IntimaTranscription Factor DP1Cell DivisionRetinoblastoma-Binding Protein 1Transcription FactorsCirculation research
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