Search results for "script"

showing 10 items of 5143 documents

Epigenetic changes and nuclear factor-κB activation, but not microRNA-224, downregulate Raf-1 kinase inhibitor protein in triple-negative breast canc…

2015

Raf-1 kinase inhibitor protein (RKIP) is a tumor suppressor and metastasis inhibitor, which enhances drug-induced apoptosis of cancer cells. Downregulation of RKIP may be significant in the biology of highly aggressive and drug-resistant tumors, for example triple-negative breast cancers (TNBCs). Potential causes for the low levels of RKIP expressed by SUM 159 TNBC cells were investigated in the present study. Bisulphite modification, methylation specific-polymerase chain reaction (PCR) and a TransAM NF-κB assay were performed and the results suggested that various mechanisms, including methylation of the gene promoter, histone deacetylation and nuclear factor-κB (NF-κB) activation, but not…

Cancer Researchmedicine.drug_classCell growthtriple-negative breast cancer Raf-1 kinase inhibitor protein epigenetic changes microRNA-224 nuclear factor-κBHistone deacetylase inhibitorArticlesCell cycleBiologyMolecular biologyDemethylating agentchemistry.chemical_compoundTrichostatin AOncologychemistryCancer cellmedicineCancer researchGrowth inhibitionTranscription factormedicine.drug
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Stimulation of endothelial nitric oxide synthase by proinsulin C-peptide.

2003

There is increasing evidence for biological functions of human C-peptide. Recently, we have described that proinsulin C-peptide increases nutritive capillary blood flow and restores erythrocyte deformability in type 1 diabetic patients, whereas it has no such effect in non-diabetic subjects. The aim of the current study was to elucidate cellular mechanisms of this vasodilator effect in vitro by measuring the nitric oxide (NO)-mediated increase of cGMP production in a RFL-6 reporter cell assay and by demonstrating endothelial calcium influx with the Fluo-3 technique. C-peptide increased the release of NO from endothelial NO synthase (eNOS) in bovine aortic endothelial cells in a concentratio…

Cancer Researchmedicine.medical_specialtyArginineNitric Oxide Synthase Type IIIPhysiologyClinical BiochemistryBlotting WesternStimulationVasodilationBiologyNitric OxideBiochemistryNitroarginineNitric oxidechemistry.chemical_compoundEnosInternal medicinemedicineErythrocyte deformabilityAnimalsHumansEnzyme InhibitorsCyclic GMPProinsulinFluorescent DyesAniline CompoundsC-PeptideC-peptideReverse Transcriptase Polymerase Chain ReactionEndothelial Cellsbiology.organism_classificationEndocrinologychemistryMicroscopy FluorescenceXanthenesRNACalciumCattleNitric Oxide SynthaseNitric oxide : biology and chemistry
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The aryl hydrocarbon receptor (AhR) in the regulation of cell–cell contact and tumor growth

2010

The aryl hydrocarbon receptor (AhR) is a ligand-dependent transcription factor, which is activated by a large group of environmental pollutants including polycyclic aromatic hydrocarbons, dioxins and planar polychlorinated biphenyls. Ligand binding leads to dimerization of the AhR with aryl hydrocarbon receptor nuclear translocator and transcriptional activation of several xenobiotic phase I and phase II metabolizing enzymes, such as cytochrome P4501A1 and glutathione- S -transferase, respectively. Since phase I enzymes convert inert carcinogens to active genotoxins, the AhR plays a key role in tumor initiation. Besides this classical route, the AhR mediates tumor promotion and recent evide…

Cancer Researchmedicine.medical_specialtyAryl hydrocarbon receptor nuclear translocatorReviewsTumor initiationCell Communicationmedicine.disease_causeInternal medicineNeoplasmsmedicineCell AdhesionHomeostasisHumansTranscription factorbiologyCell CycleCell MembraneContact inhibitionMembrane ProteinsEpithelial CellsGeneral MedicineAryl hydrocarbon receptorEndocrinologyReceptors Aryl HydrocarbonTumor progressionbiology.proteinCancer researchTumor promotionCarcinogenesisCell DivisionSignal Transduction
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Do not stress, just differentiate: role of stress proteins in hematopoiesis

2015

Hematopoiesis permits the constant regeneration of the blood system and is a permanent example of cell differentiation. Defects in its tight regulation can lead to either cell death or abnormal proliferation and may translate into multiple types of blood disorders, including leukemia. Heat shock proteins (HSPs), the expression of which is controlled by heat shock factors (HSFs, currently four known members),1 are a set of highly conserved proteins induced in response to a wide variety of physiological and environmental stress. HSP/HSF overexpression or mislocalization has been described in many cancers, particularly in hematology, and other diseases. Therefore, the involvement of HSFs/HSPs …

Cancer Researchmedicine.medical_specialtyCellular differentiationImmunologyBiologyMiceCellular and Molecular NeuroscienceHeat Shock Transcription FactorsInternal medicineHeat shock proteinmedicineAnimalsProtein IsoformsRNA MessengerHeat shockTranscription factorHeat-Shock ProteinsHematologyCell DifferentiationNews and CommentaryCell BiologyHematopoiesisCell biologyDNA-Binding ProteinsHeat shock factorHaematopoiesisCaspasesHSP60Heat-Shock ResponseTranscription FactorsCell Death & Disease
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Key lncRNAs involved in ischemic strokes

2022

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Cancer Researchmedicine.medical_specialtyIschemic strokesBiologymedicine.diseaseBrain Ischemiaischemic stroke lncRNAs miRNAs RNA transcripts stroke Humans Brain Ischemia Ischemic Stroke RNA Long NoncodingInternal medicineIschemic strokeGeneticsKey (cryptography)medicineCardiologyHumansRNA Long NoncodingStrokeIschemic StrokeEpigenomics
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TCDD-dependent downregulation of gamma-catenin in rat liver epithelial cells (WB-F344).

2002

TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin) is the most potent tumor promoter ever tested in rodents. Although it is known that most of the effects of TCDD 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 a characteristic hallmark in tumorigenesis. In WB-F344 cells, TCDD induces a release from contact-inhibition manifested by a 2- to 3-fold increase in DNA-synthesis and the emergence of foci when TCDD (1 nM) is given to confluent cells. We focussed our interest on potential cell membrane proteins mediating contact-inhibition in WB-F344 cells, namely E-cadherin, alpha,- beta,-…

Cancer Researchmedicine.medical_specialtyPolychlorinated DibenzodioxinsTime FactorsOctoxynolBlotting WesternDetergentsDown-RegulationDownregulation and upregulationInternal medicinemedicineAnimalsFluorescent Antibody Technique IndirectCells Culturedbeta CateninConfluencybiologyReverse Transcriptase Polymerase Chain ReactionLiver NeoplasmsContact inhibitionEpithelial CellsDNAAryl hydrocarbon receptorActin cytoskeletonBlotting NorthernCadherinsCell biologyRatsCytoskeletal ProteinsEndocrinologyPhenotypeOncologyDesmoplakinsLiverMicroscopy FluorescenceCateninMutationbiology.proteinProteasome inhibitorCarcinogensTrans-ActivatorsTumor promotionEnvironmental Pollutantsgamma CateninCell Divisionalpha Cateninmedicine.drugInternational journal of cancer
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Nuclear insulin receptor substrate 1 interacts with estrogen receptor alpha at ERE promoters.

2004

Insulin receptor substrate 1 (IRS-1) is a major signaling molecule activated by the insulin and insulin-like growth factor I receptors. Recent data obtained in different cell models suggested that in addition to its conventional role as a cytoplasmic signal transducer, IRS-1 has a function in the nuclear compartment. However, the role of nuclear IRS-1 in breast cancer has never been addressed. Here we report that in estrogen receptor alpha (ERalpha)-positive MCF-7 cells, (1) a fraction of IRS-1 was translocated to the nucleus upon 17-beta-estradiol (E2) treatment; (2) E2-dependent nuclear translocation of IRS-1 was blocked with the antiestrogen ICI 182,780; (3) nuclear IRS-1 colocalized and…

Cancer Researchmedicine.medical_specialtyTranscription Geneticmedicine.medical_treatmentBlotting WesternEstrogen receptorBiologyInsulin-like growth factorInternal medicineCell Line TumorGeneticsmedicineAnimalsHumansReceptorPromoter Regions GeneticMolecular BiologyNuclear receptor co-repressor 1DNA PrimersBase SequenceReverse Transcriptase Polymerase Chain ReactionEstrogen Receptor alphaPromoterAntiestrogenPhosphoproteinsPrecipitin TestsIRS1Cell biologyProtein TransportEndocrinologyNuclear receptorReceptors EstrogenInsulin Receptor Substrate ProteinsProtein BindingOncogene
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Expression and regulation by interferon-γ of the membrane-bound complement regulators CD46 (MCP), CD55 (DAF) and CD59 in gastrointestinal tumours

1999

The membrane-bound complement inhibitors CD46 (membrane cofactor protein), CD55 (decay-accelerating factor) and CD59 (protectin) protect tumour cells against lysis by activated complement. In this study, a total of 14 (3 gastric, 3 colonic and 8 pancreatic) gastrointestinal tumour cell lines were examined for the expression of CD46, CD55 and CD59 with respect to the regulatory efficacy of interferon-gamma (IFN-gamma). The effects of IFN-gamma on mRNA and protein expression levels of CD46, CD55 and CD59 were evaluated by Northern blot hybridisation, RT-PCR, flow cytometry and immunostaining. In unstimulated cell lines, CD46 and CD59 transcripts were expressed at comparable levels, whereas th…

Cancer Researchmedicine.medical_treatmentCD59 AntigensCD59BiologyMembrane Cofactor ProteinInterferon-gammaComplement inhibitorComplement Inactivator ProteinsAntigens CDmedicineHumansRNA MessengerNorthern blotGastrointestinal NeoplasmsComplement Inactivator ProteinsMembrane GlycoproteinsCD55 AntigensReverse Transcriptase Polymerase Chain ReactionCD46Blotting NorthernFlow CytometryBlotBlotting SouthernCytokineOncologyCancer researchImmunostainingEuropean Journal of Cancer
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Autocrine production of interleukin-4 and interleukin-10 is required for survival and growth of thyroid cancer cells.

2006

AbstractAlthough CD95 and its ligand are expressed in thyroid cancer, the tumor cell mass does not seem to be affected by such expression. We have recently shown that thyroid carcinomas produce interleukin (IL)-4 and IL-10, which promote resistance to chemotherapy through the up-regulation of Bcl-xL. Here, we show that freshly purified thyroid cancer cells were completely refractory to CD95-induced apoptosis despite the consistent expression of Fas-associated death domain and caspase-8. The analysis of potential molecules able to prevent caspase-8 activation in thyroid cancer cells revealed a remarkable up-regulation of cellular FLIPL (cFLIPL) and PED/PEA-15, two antiapoptotic proteins whos…

Cancer Researchmedicine.medical_treatmentNF-KAPPA-BOligonucleotidesC-FLIPCASP8 and FADD-Like Apoptosis Regulating ProteinApoptosisSuppressor of Cytokine Signaling ProteinsSIGNALING COMPLEXThyroid cancerTumorCARCINOMA CELLSANDROGEN RECEPTORIntracellular Signaling Peptides and ProteinsInterleukinHASHIMOTOS-THYROIDITISMiddle AgedProtein-Tyrosine KinasesInterleukin-10Up-RegulationMALIGNANT GLIOMA-CELLSInterleukin 10CytokineOncologyAged; Antibodies; Apoptosis; CASP8 and FADD-Like Apoptosis Regulating Protein; Cell Growth Processes; Cell Line Tumor; Humans; Interleukin-10; Interleukin-4; Intracellular Signaling Peptides and Proteins; Janus Kinase 1; Middle Aged; Oligonucleotides Antisense; Phosphoproteins; Protein-Tyrosine Kinases; Repressor Proteins; STAT6 Transcription Factor; Suppressor of Cytokine Signaling 1 Protein; Suppressor of Cytokine Signaling Proteins; Thyroid Neoplasms; Up-Regulation; fas Receptor; Oncology; Cancer Researchmedicine.medical_specialtyANTIAPOPTOTIC PROTEINSCell Growth ProcessesAntibodiesCell LineThyroid carcinomaSuppressor of Cytokine Signaling 1 ProteinSettore MED/04 - PATOLOGIA GENERALEInternal medicineCell Line TumormedicineHumansThyroid Neoplasmsfas ReceptorAntisenseAutocrine signallingInterleukin 4AgedAPOPTOSIS-INDUCING LIGANDbusiness.industryJanus Kinase 1Oligonucleotides Antisensemedicine.diseasePhosphoproteinsRepressor ProteinsEndocrinologyCancer cellCancer researchInterleukin-4businessApoptosis Regulatory ProteinsSTAT6 Transcription FactorCancer research
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Expression pattern of the urokinase-plasminogen activator system in rat DS-sarcoma: Role of oxygenation status and tumour size

2002

The urokinase plasminogen activator system plays a central role in malignant tumour progression. Both tumour hypoxia and enhancement of urokinase plasminogen activator, urokinase plasminogen activator-receptor and plasminogen activator inhibitor type 1 have been identified as adverse prognostic factors. Upregulation of urokinase plasminogen activator or plasminogen activator inhibitor type 1 could present means by which hypoxia influences malignant progression. Therefore, the impact of hypoxia on the expression pattern of the urokinase plasminogen activator system in rat DS-sarcoma in vivo and in vitro was examined. In the in vivo setting, tumour cells were implanted subcutaneously into rat…

Cancer Researchplasminogen activator inhibitor type-1DS-sarcomaEnzyme-Linked Immunosorbent AssayReceptors Cell Surfaceurokinase plasminogen activator receptorBiologyReceptors Urokinase Plasminogen Activatorchemistry.chemical_compoundDownregulation and upregulationIn vivoPlasminogen Activator Inhibitor 1Tumor Cells CulturedmedicineAnimalsExperimental TherapeuticsZymographyRNA Messengerurokinase plasminogen activatorHyperoxiaUrokinasehypoxiaReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingSarcomamalignant progressionUrokinase-Type Plasminogen ActivatorMolecular biologyIn vitroRatsGene Expression Regulation NeoplasticOxygenUrokinase receptorOncologychemistryOrgan SpecificityPlasminogen activator inhibitor-1medicine.symptommedicine.drugBritish Journal of Cancer
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