Search results for "TUMOR CELLS"

showing 10 items of 663 documents

E-selectin modulates the malignant properties of T84 colon carcinoma cells.

2002

The extravasation of metastatic cells is regulated by molecular events involving the initial adhesion of tumor cells to the endothelium and subsequently the migration of cells in the host connective tissue. E-selectin on endothelial cells and sialyl Lewis X carbohydrate component on tumor cells are mainly involved in the adhesion of colon carcinoma cells to the endothelium of target organ. Interaction of T84 colon cancer cells to purified E-selectin in vitro caused an increase in the tyrosine phosphorylation of a number of proteins as well as the modulation of cellular properties correlated to the metastatic phenotype. Specifically, E-selectin-stimulated actin reorganization, increased coll…

EndotheliumLactams MacrocyclicBiophysicsOligosaccharidesBiologyBiochemistryCell–cell interactionCancer stem cellCell MovementE-selectinmedicineBenzoquinonesCell AdhesionTumor Cells CulturedHumansEnzyme InhibitorsNeoplasm MetastasisPhosphorylationCell adhesionPhosphotyrosineSialyl Lewis X AntigenMolecular BiologyCells CulturedCarcinomaSoluble cell adhesion moleculesQuinonesCell migrationCell BiologyProtein-Tyrosine KinasesPhosphoproteinsCoculture TechniquesCell biologymedicine.anatomical_structureRifabutinCancer cellColonic NeoplasmsCancer researchbiology.proteinMatrix Metalloproteinase 2Endothelium VascularE-SelectinBiochemical and biophysical research communications
researchProduct

Phenoloxidase-dependent cytotoxic mechanism in ascidian (Styela plicata) hemocytes active against erythrocytes and K562 tumor cells.

1997

The cytotoxic activity against rabbit erythrocytes (RE) and human K562 tumor cells by Styela plicata hemocytes was significantly related to the phenoloxidase (PO) which converts phenols to quinone and initiates the melanogenic pathway. The effector hemocyte population, separated in a Percoll density gradient band, enriched in a granulocyte type named "morula cells", was examined with RE in a hemocyte cytotoxic assay and plaque forming cell assay. Inhibition experiments with the copper chelating agents 1-phenyl-2-thiourea and tropolone, the substrate analogue sodium benzoate and sodium ascorbate support the notion that hemocyte cytotoxic activity is a PO-dependent mechanism. Treatments of he…

ErythrocytesHemocytesMonophenol MonooxygenaseCytotoxicitySettore BIO/05 - ZoologiaHemocyteHydrogen PeroxideTunicateCell FractionationNitric OxidePhenylthioureaTropoloneErythrocytePhenoloxidaseCentrifugation Density GradientTumor Cells CulturedAnimalsHumansQuinoneRabbitsUrochordataK562Settore BIO/06 - Anatomia Comparata E CitologiaReactive Oxygen SpeciesEuropean journal of cell biology
researchProduct

Exosome Involvment in Hsp60 secretion by tumor cells.

2011

Exosomes Hsp60 tumor cells
researchProduct

The CD95/CD95 ligand system is not the major effector in anticancer drug-mediated apoptosis.

1998

Many anticancer drugs are able to induce apoptosis in tumor cells but the mechanisms underlying this phenomenon are poorly understood. Some authors reported that the p53 tumor suppressor gene may be responsible for drug-induced apoptosis; however, chemotherapy-induced apoptosis can also be observed in p53 negative cells. Recently, doxorubicin (DXR) was reported to induce CD95L expression to mediate apoptosis through the CD95/CD95L system. Thus, an impairment of such a system may be involved in drug resistance. We evaluated the in vitro antitumor activity of several cytotoxic drugs on two human p53-negative T-cell lymphoma cell lines, the HUT78-B1 CD95L-resistant cell line and the HUT78 pare…

Fas Ligand ProteinCaspase 3Antineoplastic AgentsApoptosismedicineTumor Cells CulturedCytotoxic T cellHumansfas ReceptorCytotoxicityMolecular BiologyEtoposideEtoposideMembrane GlycoproteinsChemistryCaspase 3Cell BiologyFas receptorCaspase InhibitorsProto-Oncogene Proteins c-bcl-2Cell cultureApoptosisDoxorubicinCaspasesCancer researchTumor Suppressor Protein p53Camptothecinmedicine.drugCell death and differentiation
researchProduct

Oxidative stress induces the expression of the major histocompatibility complex in murine tumor cells.

2001

The effect of t-butyl hydroperoxide (t-BOOH) on the induction of the Major Histocompatibility Complex (MHC) class I genes has been studied in two cell clones (B9 and G2) of the methylcholanthrene-induced murine fibrosarcoma GR9. These two clones were selected based on their different biological and biochemical behavior specially related to their tumor induction capability when injected into a BALB/c mouse. t-BOOH (0.125 mM) induced the expression of H-2 molecules in both cell clones. In B9 cell clone, in which MHC basal expression is very low or absent, t-BOOH significantly induced H-2Kd, H-2Dd and H-2Ld molecules. In G2 cell clone the expression of MHC class I genes was also enhanced by th…

FibrosarcomaCellElectrophoretic Mobility Shift AssayBiologyMajor histocompatibility complexBiochemistryMajor Histocompatibility ComplexTransactivationMiceAntigentert-ButylhydroperoxideCell CloneMalondialdehydeMHC class ImedicineTumor Cells CulturedAnimalsGlutathione PeroxidaseMice Inbred BALB CSuperoxide DismutaseMHC Class I GeneHistocompatibility Antigens Class INF-kappa BDeoxyguanosineGeneral Medicine3T3 CellsCatalaseFlow CytometryMolecular biologyGlutathioneOxidative Stressmedicine.anatomical_structureGene Expression Regulation8-Hydroxy-2'-Deoxyguanosinebiology.proteinCD8MethylcholanthreneFree radical research
researchProduct

Influence of Pharmacokinetic Variations on the Pharmacological Properties of Adriamycin

1972

Whenever it appears impossible to modify the chemical structure of drugs with a high and established therapeutic activity but a low chemotherapeutic index, pharmacological research has to find other ways of improving the chemotherapeutic index. This problem is particularly important in the case of antitumor drugs, thus justifying research into the most suitable choice of dosage and routes of administration, as well as into the pharmacological associations which enable tumor cells to be hit at various stages of the reproductive cycle. Alternatively, the therapeutic index could be improved by the use of antagonistic compounds (like, for example, methotrexate and folinic acid) which act upon t…

Folinic acidTherapeutic indexPharmacokineticsbusiness.industryPharmacological researchMedicineTumor cellsMethotrexateAortic flowPharmacologybusinessReproductive cyclemedicine.drug
researchProduct

Apoptosis induced in hepatoblastoma HepG2 cells by the proteasome inhibitor MG132 is associated with hydrogen peroxide production, expression of Bcl-…

2002

This report is focused on the apoptotic effect induced by MG132, an inhibitor of 26S proteasome, in human hepatoma HepG2 cells. The results were compared with those obtained with non-transformed human Chang liver cells. MG132 reduced the viability of HepG2 cells in a time- and dose-dependent manner. The effect was in tight connection with the induction of apoptosis, as indicated by fluorescence microscopy and cytometric analysis, and was accompanied by a remarkable increase in the production of H2O2 and a reduction in mitochondrial transmembrane potential (Deltapsim). In addition cell death was prevented by antioxidants such as GSH, N-acetylcysteine or catalase. Western blot analysis showed…

G2 PhaseHepatoblastomaCancer ResearchProgrammed cell deathProteasome Endopeptidase ComplexMG132Time FactorsCell SurvivalLeupeptinsPoly ADP ribose polymeraseBlotting Westernbcl-X ProteinMitosisCaspase 3Antineoplastic AgentsApoptosismacromolecular substancesMembrane Potentialschemistry.chemical_compoundCytosolMultienzyme ComplexesMG132medicineTumor Cells CulturedHumansCaspasebiologyCaspase 3Cytochrome cCell CycleLiver NeoplasmsHydrogen PeroxideFlow CytometryMolecular biologyMitochondriaEnzyme ActivationCysteine EndopeptidasesOxidative StressOncologyBiochemistrychemistryProto-Oncogene Proteins c-bcl-2ApoptosisCaspasesbiology.proteinProteasome inhibitormedicine.drug
researchProduct

Cellular uptake and in vitro antitumor efficacy of composite liposomes for neutron capture therapy.

2014

Background Neutron capture therapy for glioblastoma has focused mainly on the use of 10B as neutron capture isotope. However, 157Gd offers several advantages over boron, such as higher cross section for thermal neutrons and the possibility to perform magnetic resonance imaging during neutron irradiation, thereby combining therapy and diagnostics. We have developed different liposomal formulations of gadolinium-DTPA (Magnevist®) for application in neutron capture therapy of glioblastoma. The formulations were characterized physicochemically and tested in vitro in a glioma cell model for their effectiveness. Methods Liposomes entrapping gadolinium-DTPA as neutron capture agent were manufactur…

Gadolinium DTPANeutronsDrug uptakeBrain NeoplasmsResearchContrast MediaGadoliniumGliomaNeutron Capture TherapyIn Vitro TechniquesMagnetic Resonance ImagingTheranosticLiposomesTumor Cells CulturedHumansMonte Carlo MethodCell ProliferationRadiation oncology (London, England)
researchProduct

Proliferation of gastrointestinal carcinoma cells by T lymphocyte factors interleukin-3 and granulocyte-macrophage colony-stimulating factor

1991

Hematopoietic growth factors have been well characterized by cDNA cloning in recent years. In order to determine the influence of rhGM-CSF and rhIL-3 on epithelial cells of the gastrointestinal tract, their influence on in vitro cultured gastric and pancreas cancer cells was determined. A more than two-fold enhancement of proliferation was observed by IL-3 and GM-CSF in Mz-Sto-1 gastric and 818-4 pancreas carcinoma cells, applying a sensitive microculture system which allows precise quantification. The highest growth rates were obtained adding 1-10 ng/ml of the growth factors, but even picogram amounts were effective. Expression of mRNA for GM-CSF and IL-3 remained undetectable in the cell …

Gastrointestinal tractT-LymphocytesImmunologyGranulocyte-Macrophage Colony-Stimulating FactorBiologyLymphocyte ActivationMolecular biologyIn vitroPancreatic NeoplasmsHaematopoiesisGranulocyte macrophage colony-stimulating factorStomach NeoplasmsCell cultureCancer cellTumor Cells CulturedmedicineHumansInterleukin-3ReceptorCell DivisionInterleukin 3medicine.drugImmunologic Research
researchProduct

Urokinase Plasminogen Activator and Gelatinases Are Associated with Membrane Vesicles Shed by Human HT1080 Fibrosarcoma Cells

1997

Membrane vesicles are shed by tumor cells both in vivo and in vitro. Although their functions are not well understood, it has been proposed that they may play multiple roles in tumor progression. We characterized membrane vesicles from human HT1080 fibrosarcoma cell cultures for the presence of proteinases involved in tumor invasion. By gelatin zymography and Western blotting, these vesicles showed major bands corresponding to the zymogen and active forms of gelatinase B (MMP-9) and gelatinase A (MMP-2) and to the MMP-9. tissue inhibitor of metalloproteinase 1 complex. Both gelatinases appeared to be associated with the vesicle membrane. HT1080 cell vesicles also showed a strong, plasminoge…

GelatinasesMacromolecular SubstancesFibrosarcomaBlotting WesternCellGelatinase ABiologyBiochemistryTumor Cells CulturedmedicineHumansCollagenasesFibrinolysinMolecular BiologyGlycoproteinsUrokinaseEnzyme PrecursorsVesicleMetalloendopeptidasesTissue Inhibitor of MetalloproteinasesCell BiologyTissue inhibitor of metalloproteinaseUrokinase-Type Plasminogen ActivatorMolecular biologyExtracellular MatrixUrokinase receptorBloodmedicine.anatomical_structureMatrix Metalloproteinase 9GelatinasesMatrix Metalloproteinase 2HT1080medicine.drugJournal of Biological Chemistry
researchProduct