Search results for "CELL SURVIVAL"

showing 10 items of 870 documents

Tumour-derived and host-derived nitric oxide differentially regulate breast carcinoma metastasis to the lungs.

2004

To study the role of nitric oxide (NO) in lung metastasis of breast carcinoma, we isolated two cell clones (H and J) from the parental EMT-6 murine breast carcinoma cell line, based on their differential NO production. In vitro, EMT-6 J cells, but not EMT-6H cells, constitutively expressed inducible NO synthase (NOS II) and secreted high levels of NO. IL-1beta increased NO production in both clones, and TNF-alpha had a synergistic effect on IL-1beta-induced NO production, but NO production by EMT-6 J cells was always higher than by EMT-6H cells. Proliferation, survival and adhesion to lung-derived endothelial cells of both clones were similar and were not affected by NO. In vivo, both clone…

Cancer ResearchPathologymedicine.medical_specialtyLung NeoplasmsCell SurvivalCellNitric Oxide Synthase Type IINitric OxideGuanidinesNitric oxideMetastasischemistry.chemical_compoundMiceCarcinomamedicineCell AdhesionTumor Cells CulturedAnimalsEnzyme InhibitorsCell adhesionMice KnockoutMice Inbred BALB CbiologyIndium RadioisotopesEndothelial CellsMammary Neoplasms ExperimentalGeneral Medicinemedicine.diseaseIn vitroNitric oxide synthaseMice Inbred C57BLSurvival Ratemedicine.anatomical_structurechemistryCell cultureembryonic structuresCancer researchbiology.proteinFemaleNitric Oxide SynthaseCell DivisionAnimals/Cell Adhesion/Cell Division/Cell Survival/Endothelial Cells/metabolism/Pathology/Enzyme Inhibitors/pharmacology/Female/Guanidines/Indium Radioisotopes/Interleukin-1/Lung Neoplasms/enzymology/secondary/Mammary NeoplasmsExperimental/Mice/MiceInbred BALB C/MiceInbred C57BL/MiceKnockout/Nitric Oxide/physiology/Nitric Oxide Synthase/antagonists & inhibitors/Nitric Oxide Synthase Type II/Survival Rate/Tumor CellsCulturedInterleukin-1Carcinogenesis
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Development of resistance towards artesunate in MDA-MB-231 human breast cancer cells.

2011

Breast cancer is the most common cancer and the second leading cause of cancer death in industrialized countries. Systemic treatment of breast cancer is effective at the beginning of therapy. However, after a variable period of time, progression occurs due to therapy resistance. Artesunate, clinically used as anti-malarial agent, has recently revealed remarkable anti-tumor activity offering a role as novel candidate for cancer chemotherapy. We analyzed the anti-tumor effects of artesunate in metastasizing breast carcinoma in vitro and in vivo. Unlike as expected, artesunate induced resistance in highly metastatic human breast cancer cells MDA-MB-231. Likewise acquired resistance led to abol…

Cancer ResearchPhytochemistryPhytopharmacologyCancer TreatmentArtesunateApoptosisElectrophoretic Mobility Shift AssayDrug resistanceNude MiceMetastasischemistry.chemical_compoundMiceMolecular Cell BiologyDrug DiscoveryBreast TumorsBasic Cancer ResearchMedicinebcl-2-Associated X ProteinMultidisciplinaryQRNF-kappa BArtemisininsChemistryOncologyMedicineFemaleMatrix Metalloproteinase 1Breast carcinomamedicine.drugResearch Article570Drugs and DevicesDrug Research and DevelopmentCell SurvivalScienceMice Nude570 Life SciencesBreast NeoplasmsTumor Cell Line610 Medical Sciences MedicineBreast cancerComplementary and Alternative MedicineCell Line TumorAnimalsHumansDoxorubicinBiologyNeoplasm Drug Resistancebusiness.industryCancers and NeoplasmsChemotherapy and Drug Treatmentmedicine.diseaseXenograft Model Antitumor AssaysTranscription Factor AP-1chemistryTumor progressionArtesunateDrug Resistance NeoplasmCancer cellImmunologyEthnopharmacologyCancer researchbusinessPloS one
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Effective infection, apoptotic cell killing and gene transfer of human hepatoma cells but not primary hepatocytes by parvovirus H1 and derived vector…

2001

Autonomous parvoviruses preferentially replicate in and kill in vitro–transformed cells and reduce the incidence of spontaneous and implanted tumors in animals. Because of these natural oncotropic and oncolytic properties, parvoviruses deserve to be considered as potential antitumor vectors. Here, we assessed whether parvovirus H1 is able to kill human hepatoma cells by induction of apoptosis but spares primary human liver cells, and whether the former cells can efficiently be transduced by H1 virus–based vectors. Cell death, infectivity, and transgene transduction were investigated in Hep3B, HepG2, and Huh7 cells and in primary human hepatocytes with natural and recombinant H1 virus. All h…

Cancer ResearchProgrammed cell deathCarcinoma HepatocellularParvovirus H-1Cell SurvivalvirusesGenetic VectorsApoptosisVirus ReplicationVirusCell LineParvoviridae InfectionsParvovirusTransduction (genetics)Transduction GeneticTumor Cells CulturedHumansMolecular BiologybiologyParvovirusLiver NeoplasmsGene Transfer Techniquesbiology.organism_classificationVirologyMolecular biologydigestive system diseasesOncolytic virusCell killingApoptosisDNA ViralHepatocytesMolecular MedicineCancer gene therapy
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Sodium phenylbutyrate induces apoptosis in human retinoblastoma Y79 cells: The effect of combined treatment with the topoisomerase I-inhibitor topote…

2001

Our results demonstrate that sodium phenylbutyrate, a compound with a low degree of toxicity, exerted a cytotoxic effect on human retinoblastoma Y79 cells in a time- and dose-dependent manner. Treatment of Y79 cells for 72 h with phenylbutyrate reduced cell viability by 63% at 2 mM and 90% at 4 mM. Cell death caused by phenylbutyrate exhibited the typical features of apoptosis, as shown by light and fluorescent microscopy. Western blot analysis demonstrated that exposure of Y79 cells to phenylbutyrate decreased the level of the antiapoptotic factor Bcl-2 and induced the activation of caspase-3, a key enzyme in the execution phase of apoptosis. Moreover, treatment with phenylbutyrate markedl…

Cancer ResearchProgrammed cell deathCell SurvivalBlotting WesternApoptosisPhenylbutyrateHistonesSettore BIO/10 - BiochimicamedicineTumor Cells CulturedHumansretinoblastoma apoptosis sodium phenylbutirateViability assayEnzyme InhibitorsbiologyCaspase 3TopoisomeraseRetinoblastomaSodium phenylbutyrateAcetylationDrug SynergismCell cyclePhenylbutyrateseye diseasesEnzyme ActivationOncologyProto-Oncogene Proteins c-bcl-2ApoptosisCaspasesbiology.proteinCancer researchTopotecanDrug Therapy CombinationTopoisomerase I InhibitorsTumor Suppressor Protein p53Topotecanmedicine.drug
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Nupr1-Aurora Kinase A Pathway Provides Protection against Metabolic Stress-Mediated Autophagic-Associated Cell Death

2012

Abstract Purpose: The limited supply of oxygen and nutrients is thought to result in rigorous selection of cells that will eventually form the tumor. Experimental Design: Nupr1 expression pattern was analyzed in human tissue microarray (TMA) and correlated with survival time of the patient. Microarray analysis was conducted on MiaPaCa2 cells subjected to metabolic stress in Nupr1-silenced conditions. DNA repair and cell cycle–associated gene expression was confirmed by real-time quantitative PCR (qRT-PCR). Nupr1 and AURKA protective role were analyzed using RNA interference (RNAi) silencing or overexpression. DNA damage and autophagy were analyzed by Western blot analysis and immunofluoresc…

Cancer ResearchProgrammed cell deathCell SurvivalDNA damageDNA repairAdenocarcinomaProtein Serine-Threonine KinasesBiologyAurora KinasesStress PhysiologicalCell Line TumorAutophagyBasic Helix-Loop-Helix Transcription FactorsHumansGene silencingAurora Kinase ARegulation of gene expressionGene knockdownMicroarray analysis techniquesAURKA GeneMolecular biologyCell HypoxiaNeoplasm ProteinsCell biologyGene Expression Regulation NeoplasticGlucoseOncologyRNA InterferenceCarcinoma Pancreatic DuctalClinical Cancer Research
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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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Lovastatin protects human endothelial cells from killing by ionizing radiation without impairing induction and repair of DNA double-strand breaks.

2006

Abstract Purpose: 3-hydroxy-3-methylglutaryl CoA reductase inhibitors (statins) are frequently used lipid-lowering drugs. Moreover, they are reported to exert pleiotropic effects on cellular stress responses, proliferation, and apoptosis. Whether statins affect the sensitivity of primary human cells to ionizing radiation (IR) is still unknown. The present study aims at answering this question. Experimental Design: The effect of lovastatin on IR-provoked cytotoxicity was analyzed in primary human umbilical vein endothelial cells (HUVEC). To this end, cell viability, proliferation, and apoptosis as well as DNA damage–related stress responses were investigated. Results: The data show that lova…

Cancer ResearchProgrammed cell deathDNA RepairDNA repairDNA damageCell SurvivalApoptosisRadioresistanceRadiation Ionizingpolycyclic compoundsmedicineHumansLovastatinCells CulturedCell Proliferationbiologynutritional and metabolic diseasesEndothelial CellsDose-Response Relationship RadiationDNAMolecular biologyEndothelial stem cellOncologyApoptosisCytoprotectionHMG-CoA reductasebiology.proteinCancer researchlipids (amino acids peptides and proteins)Lovastatinmedicine.drugDNA DamageClinical cancer research : an official journal of the American Association for Cancer Research
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The apoptotic effects of cisplatin and carboplatin in retinoblastoma Y79 cells.

1998

This study demonstrated that cisplatin and carboplatin stimulate apoptosis in human retinoblastoma Y79 cells, cisplatin being the most effective compound. The apoptotic effect appeared after 8 h and then increased in a time-dependent manner. Treatment with cisplatin and carboplatin also provoked an increase in the level of p53 and p21, and a lowering in Bcl-2. The prolonged exposure of Y79 cells to cisplatin induced resistance to cisplatin, carboplatin and etoposide. The basal level of p53 was in resistant cells higher than in untreated cells, while Bcl-2 was not modified. p53 and Bcl-2 levels did not change after treating of resistant cells with cisplatin, carboplatin or etoposide. However…

Cancer ResearchProgrammed cell deathPathologymedicine.medical_specialtyCell Survivalmedicine.medical_treatmentAntineoplastic AgentsApoptosisBiologychemistry.chemical_compoundTumor Cells CulturedmedicineHumansEtoposideCisplatinChemotherapyRetinoblastomaDNA NeoplasmCarboplatinProto-Oncogene Proteins c-bcl-2OncologychemistryDrug Resistance NeoplasmApoptosisCell culturecarboplatinCancer researchCisplatinTumor Suppressor Protein p53Camptothecinmedicine.drugInternational Journal of Oncology
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The role of oxidative stress in apoptosis induced by the histone deacetylase inhibitor suberoylanilide hydroxamic acid in human colon adenocarcinoma …

2008

Histone deacetylase inhibitors (HDACIs) activate genes that promote cell cycle arrest and apoptosis in a number of tumor cells. This study showed that suberoylanilide hydroxamic acid (SAHA), a potent and commonly used HDACI, induced apoptosis in human colon adenocarcinoma HT-29 cells in a time- and dose-dependent manner. This effect was accompanied by the induction of oxidative stress, dissipation of mitochondrial transmembrane potential and activation of executioner caspases. Moreover, SAHA increased the levels of phosphorylated active forms of p38 and JNK. The addition of either the antioxidant N-acetylcysteine or the specific inhibitor of NADPH oxidase diphenylene iodonium chloride reduc…

Cancer ResearchProgrammed cell deathmedicine.drug_classCell Survivalp38 mitogen-activated protein kinasesBlotting WesternApoptosisAdenocarcinomamedicine.disease_causeHydroxamic AcidsAntioxidantsSettore BIO/10 - BiochimicamedicineHumansEnzyme InhibitorsProtein kinase BCaspaseMembrane Potential MitochondrialVorinostatbiologyHistone deacetylase inhibitorEnzyme ActivationHistone Deacetylase InhibitorsOxidative StressOncologyBiochemistryApoptosisCaspasesColonic NeoplasmsCancer researchbiology.proteinHistone deacetylaseReactive Oxygen Speciescolon adenomacarcinoma cells histone deacetylase inhibitors apoptosisHT29 CellsOxidative stressSignal TransductionInternational journal of oncology
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Tumor and its microenvironment: a synergistic interplay.

2013

The mutual and interdependent interaction between tumor and its microenvironment is a crucial topic in cancer research. Recently, it was reported that targeting stromal events could improve efficacies of current therapeutics and prevent metastatic spreading. Tumor microenvironment is a "complex network" of different cell types, soluble factors, signaling molecules and extracellular matrix components, which orchestrate the fate of tumor progression. As by definition, cancer stem cells (CSCs) are proposed to be the unique cell type able to maintain tumor mass and survive outside the primary tumor at metastatic sites. Being exposed to environmental stressors, including reactive oxygen species …

Cancer ResearchStromal cellEpithelial-Mesenchymal TransitionAngiogenesisCell SurvivalBiologyCancer stem cellCell MovementNeoplasmsmedicineTumor MicroenvironmentAnimalsHumansEpithelial–mesenchymal transitionNeoplasm MetastasisStem Cell NicheHypoxiaTumor microenvironmentNeovascularization Pathologicmedicine.diseaseAngiogenesis CAFs CAMs CRC CSCs ECM EMT GSH HIF Hypoxia MMPs ROS Tumor microenvironment VEGF cancer stem cells cancer-associated fibroblasts cancer-associated macrophages colorectal cancer epithelial mesenchymal transition extracellular matrix hypoxia-inducible factor matrix metalloproteinase reactive oxygen species reduced glutathione vascular endothelial growth factorPrimary tumorTumor progressionImmunologyCancer researchNeoplastic Stem CellsCancer-Associated FibroblastsOxidation-ReductionSignal Transduction
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