Search results for "Retinoblastoma Protein"

showing 10 items of 30 documents

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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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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p27Kip1participates in the regulation of endoreplication in differentiating chick retinal ganglion cells

2015

Nuclear DNA duplication in the absence of cell division (i.e. endoreplication) leads to somatic polyploidy in eukaryotic cells. In contrast to some invertebrate neurons, whose nuclei may contain up to 200,000-fold the normal haploid DNA amount (C), polyploid neurons in higher vertebrates show only 4C DNA content. To explore the mechanism that prevents extra rounds of DNA synthesis in these latter cells we focused on the chick retina, where a population of tetraploid retinal ganglion cells (RGCs) has been described. We show that differentiating chick RGCs that express the neurotrophic receptors p75 and TrkB while lacking retinoblastoma protein, a feature of tetraploid RGCs, also express p27K…

Retinal Ganglion CellsretinaEndocycleCell divisionCellular differentiationChick EmbryoRetinoblastoma ProteinendoreduplicationMicevertebrateRNA Small InterferingpolyploidyMice KnockoutRGCeducation.field_of_studyCell DifferentiationEndoreduplicationCell cycleImmunohistochemistryNuclear DNAendocycleneurogenesiscell cycleRNA InterferenceCyclin-Dependent Kinase Inhibitor p27NeurogenesisPopulationDown-RegulationCell cycleBiologyRetinal ganglionRetinaPolyploidyReportAnimalsReceptor trkBEndoreduplicationeducationMolecular BiologyPloidiesDNA synthesisVertebrateCyclin-Dependent Kinase 4Cyclin-Dependent Kinase 6Cell BiologyMinichromosome Maintenance Complex Component 7Molecular biologyeye diseasessense organsChickensDevelopmental BiologyCell Cycle
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Missing Evidences in Cancer Genetics: The Retinoblastoma Paradigm

2008

BACKGROUND: Retinoblastoma (Rb) is the most common primary malignant intraocular tumour in childhood. The "two hit" theory, formulated by Knudson in 1971 to explain the variegated clinical expression of the disease, led to the discovery of the so called tumour suppressor genes and the identification of the Rb1 as the prototype of such genes. Mutations of the Rb1 gene are now commonly believed to be the "cause" retinoblastoma, although epidemiological, clinical, and biological evidences argue against it. MATERIAL/METHODS: The Authors have performed a systematic review of available data concerning clinical and diagnostic aspects of retinoblastoma, including molecular genetics. Meta analysis o…

Retinoblastoma pRBCancer Researchlcsh:CytologyRetinoblastomaCell BiologyGeneral Medicinelcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogenslcsh:RC254-282Retinoblastoma ProteinPathology and Forensic MedicineMutationHumansMolecular MedicineGenetic Predisposition to Diseaselcsh:QH573-671Letter to the EditorCellular Oncology : the Official Journal of the International Society for Cellular Oncology
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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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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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Induction of apoptosis in human osteosarcoma Saos-2 cells by the proteasome inhibitor MG132 and the protective effect of pRb

2003

Induction of apoptosis in human osteosarcoma Saos-2 cells by the proteasome inhibitor MG132 and the protective effect of pRb

Time FactorsLeupeptinsApoptosisRetinoblastoma ProteinAntioxidantsAmino Acid Chloromethyl KetonesMembrane Potentialschemistry.chemical_compoundSettore BIO/10 - BiochimicaMG132Caspase 8OsteosarcomaChemistryCaspase 3Cytochromes cFlow CytometryMitochondriaCysteine EndopeptidasesProto-Oncogene Proteins c-bcl-2CaspasesOsteosarcomamedicine.drugmusculoskeletal diseasesProteasome Endopeptidase ComplexCell SurvivalBlotting Westernbcl-X Proteinmacromolecular substancesTransfectionMultienzyme ComplexesCell Line Tumorparasitic diseasesmedicineHumansProtease InhibitorsneoplasmsMolecular BiologySaos-2 cellsDose-Response Relationship DrugCell Biologymedicine.diseaseAcetylcysteineApoptosis osteosarcoma proteasome inhibitorsMicroscopy FluorescenceApoptosisCancer researchProteasome inhibitorTumor Suppressor Protein p53Reactive Oxygen Specieshuman activities
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The HMGA1 protoncogene frequently deregulated in cancer is a transcriptional target of E2F1

2011

Reactivation of the HMGA1 protoncogene is very frequent in human cancer, but still very little is known on the molecular mechanisms leading to this event. Prompted by the finding of putative E2F binding sites in the human HMGA1 promoter and by the frequent deregulation of the RB/E2F1 pathway in human carcinogenesis, we investigated whether E2F1 might contribute to the regulation of HMGA1 gene expression. Here we report that E2F1 induces HMGA1 by interacting with a 193bp region of the HMGA1 promoter containing an E2F binding site surrounded by three putative Sp1 binding sites. Both gain and loss of function experiments indicate that Sp1 functionally interacts with E2F1 to promote HMGA1 expre…

Transcriptional ActivationChromatin ImmunoprecipitationSp1 Transcription FactorBlotting WesternMolecular Sequence DataReal-Time Polymerase Chain ReactionRetinoblastoma ProteinSp1MiceAnimalsHumansPituitary NeoplasmsThyroid NeoplasmsHMGA1a ProteinPituitary NeoplasmRNA MessengerPromoter Regions GeneticCarcinogenesiThyroid NeoplasmHMGA1 promoterMice KnockoutBinding SitesBase SequenceAnimalReverse Transcriptase Polymerase Chain ReactionBinding SiteMutationMutagenesis Site-DirectedTranscriptionE2F1 Transcription FactorHumansp1; carcinogenesis; hmga1 promoter; transcription
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Aryl hydrocarbon receptor-dependent cell cycle arrest in isolated mouse oval cells

2013

The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor, which mediates toxic responses to environmental pollutants, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and related compounds. Besides its well known role in induction of xenobiotic metabolizing enzymes, for instance CYP1A1, the AhR is also involved in tumor promotion in rodents although the underlying mechanisms are still poorly understood. Additionally, the AhR is known to regulate cellular proliferation, which might result in either inhibition or stimulation of proliferation depending on the cell-type studied. Potential targets in hepatocarcinogenesis are liver oval (stem/progenitor) cells. In the pres…

medicine.medical_specialtyTCDDPolychlorinated DibenzodioxinsCell cycle checkpointBlotting WesternCyclin AMice TransgenicCyclin ATransfectionToxicologyRetinoblastoma ProteinCell LineMiceCyclin D1Proliferating Cell Nuclear AntigenInternal medicinemedicineAnimalsCyclin D1RNA Small InterferingTranscription factorCell Proliferationbiologyaryl hydrocarbon receptorRetinoblastoma proteinmouse oval cellsCell Cycle CheckpointsGeneral MedicineCell cycleAryl hydrocarbon receptorCell biologyEndocrinologyLiverReceptors Aryl Hydrocarbonbiology.proteinEnvironmental PollutantsTumor promotioncell cycle
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CVB3 VP1 interacts with MAT1 to inhibit cell proliferation by interfering with Cdk-activating kinase complex activity in CVB3-induced acute pancreati…

2021

Coxsackievirus B3 (CVB3) belongs to the genus Enterovirus of the family Picornaviridae and can cause acute acinar pancreatitis in adults. However, the molecular mechanisms of pathogenesis underlying CVB3-induced acute pancreatitis have remained unclear. In this study, we discovered that CVB3 capsid protein VP1 inhibited pancreatic cell proliferation and exerted strong cytopathic effects on HPAC cells. Through yeast two-hybrid, co-immunoprecipitation, and confocal microscopy, we show that Menage a trois 1 (MAT1), a subunit of the Cdk-Activating Kinase (CAK) complex involved in cell proliferation and transcription, is a novel interaction protein with CVB3 VP1. Moreover, CVB3 VP1 inhibited MAT…

virusesCultured tumor cellsSynthesis PhaseCell Cycle ProteinsBiochemistryCell Cycle and Cell DivisionBiology (General)PhosphorylationPost-Translational ModificationCyclin0303 health sciencesbiologyKinaseChemistry030302 biochemistry & molecular biologyRetinoblastoma proteinvirus diseasesCell DifferentiationTransfectionCyclin-Dependent KinasesCell biologyEnterovirus B HumanCell ProcessesPhosphorylationCell linesBiological culturesResearch ArticleQH301-705.5Protein subunitImmunologyCoxsackievirus InfectionsTransfectionResearch and Analysis MethodsMicrobiology03 medical and health sciencesVirologyCyclinsGeneticsHumansHeLa cellsMolecular Biology TechniquesMolecular Biology030304 developmental biologyCell ProliferationCell growthG1 PhaseBiology and Life SciencesProteinsCell Cycle CheckpointsCell BiologyRC581-607Cell culturesPancreatitisbiology.proteinParasitologyCapsid ProteinsImmunologic diseases. AllergyCyclin-dependent kinase 7Cyclin-Dependent Kinase-Activating KinaseTranscription FactorsPLoS pathogens
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