Search results for "FAS"

showing 10 items of 2015 documents

Cleavage of CD95 by matrix metalloproteinase-7 induces apoptosis resistance in tumour cells

2004

The ability of tumour cells to resist apoptosis-inducing signals by cytotoxic T cells may decide the success or failure of tumour elimination. An important effector of apoptosis is the CD95/CD95 ligand system (APO-1/Fas) that mediates perforin-independent cytotoxic T-cell killing of tumour cells. We propose a new strategy by which tumour cells can resist CD95-induced apoptosis. We identified matrix metalloproteinase-7, MMP-7 (Martilysin), as the first physiologically relevant protease that can specifically cleave CD95. MMP-7 is of unique importance because it is produced by the tumour cells themselves at early stages of tumour development. Microsequencing of the positions in CD95 cleaved by…

Cancer ResearchEffectorApoptosishemic and immune systemschemical and pharmacologic phenomenaBiologyMatrix metalloproteinaseFas receptorCleavage (embryo)medicine.disease_causeCell biologyApoptosisMatrix Metalloproteinase 7hemic and lymphatic diseasesTumor Cells CulturedGeneticsExtracellularmedicineHumansCytotoxic T cellfas Receptorbiological phenomena cell phenomena and immunityCarcinogenesisMolecular BiologyOncogene
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Apoptotic effects of thiazolobenzimidazole derivatives on sensitive and multidrug resistant leukaemic cells

2001

We investigated the cytotoxic activity of eight thiazolobenzimidazole derivatives on sensitive HL60 and multidrug-resistant (MDR) (HL60R) leukaemia cell lines. The antitumour effects of these compounds were compared with those of RS-TBZ, a thiazolobenzimidazole derivative, previously described in our reports, that was able to induce apoptosis more markedly in MDR cells than in the parental sensitive cell lines. Only two compounds in this study proved to have interesting effects: (a) the S-enantiomer of TBZ, that was able to induce apoptosis in MDR cells in a slightly more selective manner than TBZ (racemic form); and (b) TBZ-4-OCH3 (TBZ-4-OCH3), that showed cytotoxic and apoptotic effects o…

Cancer ResearchHL60Antineoplastic AgentsHL-60 CellsApoptosisBiologyMultidrug resistanceCaspase 8Anticancer drugschemistry.chemical_compoundAntigenCytotoxic T cellHumansLeukaemiafas ReceptorProgenitor cellLeukemiaCell CycleCaspase InhibitorsDrug Resistance MultipleMultiple drug resistanceThiazolobenzimidazoleThiazolesAnticancer drugs; Apoptosis; Leukaemia; Multidrug resistance; Thiazolobenzimidazole;OncologychemistryCell cultureApoptosisDrug Resistance NeoplasmImmunologyCancer researchBenzimidazoles
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Redistribution of CD95, DR4 and DR5 in rafts accounts for the synergistic toxicity of resveratrol and death receptor ligands in colon carcinoma cells.

2004

The natural phytoalexin resveratrol (3, 5, 4'-trihydroxystilbene) exhibits both chemopreventive and antitumor activities through a variety of mechanisms. We have shown previously that resveratrol-induced apoptosis of a human colon cancer cell line involved the redistribution of CD95 (Fas/Apo-1) into lipid rafts. Here, we show that, in colon cancer cells that resist to resveratrol-induced apoptosis, the polyphenol also induces a redistribution of death receptors into lipid rafts. This effect sensitizes these tumor cells to death receptor-mediated apoptosis. In resveratrol-treated cells, tumor necrosis factor (TNF), anti-CD95 antibodies and TNF-related apoptosis-inducing ligand (TRAIL) activa…

Cancer ResearchNystatinTime FactorsApoptosisResveratrolmedicine.disease_causeLigandsReceptors Tumor Necrosis FactorTNF-Related Apoptosis-Inducing Ligandchemistry.chemical_compoundStilbenesReceptorLipid raftCaspaseMembrane GlycoproteinsbiologyFas receptorFlow CytometryLipidsMitochondriaProto-Oncogene Proteins c-bcl-2CaspasesColonic Neoplasmslipids (amino acids peptides and proteins)Tumor necrosis factor alphaSignal Transductionmedicine.medical_specialtyBlotting WesternTransfectionMembrane MicrodomainsInternal medicineCell Line TumorGeneticsmedicineHumansfas ReceptorMolecular BiologyTumor Necrosis Factor-alphaCarcinomaLipid MetabolismAntineoplastic Agents PhytogenicReceptors TNF-Related Apoptosis-Inducing LigandEndocrinologychemistryApoptosisResveratrolCancer researchbiology.proteinCarcinogenesisApoptosis Regulatory ProteinsOncogene
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Fascin upregulation in primary head and neck squamous cell carcinoma is associated with lymphatic metastasis

2014

Fascin is an actin-bundling protein that is associated with cellular motility and cancer-cell invasion. The present study aimed to examine the expression of fascin in head and neck squamous cell carcinoma (HNSCC) and its potential use as a biomarker. In a prospective study with a median follow-up time of 48.8 months, tumor tissues, adjacent healthy tissues and cervical lymph node metastases were collected from 25 patients and analyzed by immunohistochemistry. The specimens were scored according to the intensity of fascin staining and the percentage of tumor cells stained using a semi-quantitative scoring approach; the data were analyzed and correlated with clinical follow-up observations. A…

Cancer ResearchPathologymedicine.medical_specialtymacromolecular substancesfascinhead and neck squamous cell carcinomaMetastasislymphaticmedicinemetastasisLymph nodeFascinmarkerOncogenebiologybusiness.industryCancerArticlesmedicine.diseaseHead and neck squamous-cell carcinomaLymphatic systemmedicine.anatomical_structureOncologybiology.proteinImmunohistochemistrybusinessOncology Letters
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Spontaneous and Fas-induced apoptosis of low-grade MDS erythroid precursors involves the endoplasmic reticulum

2008

Spontaneous apoptosis of bone marrow erythroid precursors accounts for the anemia that characterizes most low-grade myelodysplastic syndromes (MDS). We have shown that death of these precursors involved the Fas-dependent activation of caspase-8. To explore the pathway leading from caspase-8 activation to apoptosis, we transduced MDS bone marrow CD34(+) cells with a lentivirus encoding wild-type (WT) or endoplasmic reticulum (ER)-targeted Bcl-2 protein before inducing their erythroid differentiation. Both WT-Bcl-2 and ER-targeted Bcl-2 prevented spontaneous and Fas-dependent apoptosis in MDS erythroid precursors. ER-targeted Bcl-2 inhibited mitochondrial membrane depolarization and cytochrom…

Cancer ResearchProgrammed cell deathApoptosis[SDV.BC]Life Sciences [q-bio]/Cellular BiologyMitochondrionEndoplasmic Reticulum03 medical and health sciences0302 clinical medicinehemic and lymphatic diseasesmedicineHumansfas ReceptorErythropoietinComputingMilieux_MISCELLANEOUS030304 developmental biologyErythroid Precursor Cells0303 health sciencesbiologyCytochrome cEndoplasmic reticulumMembrane ProteinsAnemiaHematologyCaspase InhibitorsMitochondria3. Good healthCell biologyRed blood cellmedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2OncologyErythropoietinApoptosisMyelodysplastic Syndromes030220 oncology & carcinogenesisCancer researchbiology.protein[SDV.IMM]Life Sciences [q-bio]/ImmunologyCalciumBone marrowmedicine.drug
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Chemotherapy-induced apoptosis in hepatocellular carcinoma involves the p53 family and is mediatedviathe extrinsic and the intrinsic pathway

2010

We investigated the downstream mechanisms by which chemotherapeutic drugs elicit apoptosis in hepatocellular carcinoma (HCC). Genomic signatures of HCC cell lines treated with different chemotherapeutic drugs were obtained. Analyses of apoptosis pathways were performed and RNA interference was used to evaluate the role of the p53 family. Endogenous p53, p63 and p73 were upregulated in response to DNA damage by chemotherapeutic drugs. Blocking p53 family function led to chemoresistance in HCC. Stimulation and blocking experiments of the CD95-, the TNF- and the TRAIL-receptor systems revealed that cytotoxic drugs, via the p53 family members as transactivators, can trigger expression of each o…

Cancer ResearchProgrammed cell deathCarcinoma HepatocellularTumor suppressor geneDNA damagetumor suppressor protein p53membrane proteinsoligonucleotide array sequence analysiscarcinomaBiologyhepatocellularfas-associated death domain proteinAPAF1humansMembrane Potential Mitochondrialhep G2 cellsbleomycinliver neoplasmsSettore BIO/11apoptosisPrognosismitochondrialFas receptorcaspasesOncologyApoptosisbiology.proteinCancer researchMdm2membrane potentialSignal transductionPrognosis; bleomycin; caspases; membrane potential mitochondrial; oligonucleotide array sequence analysis; tumor suppressor protein p53; membrane proteins; fas-associated death domain protein; humans; liver neoplasms; hep G2 cells; apoptosis; carcinoma hepatocellularInternational Journal of Cancer
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Histone deacetylase inhibition by valproic acid down-regulates c-FLIP/CASH and sensitizes hepatoma cells towards CD95-and TRAIL receptor-mediated apo…

2005

Hepatocellular carcinoma (HCC) is highly resistant to chemotherapy, leading to a poor prognosis of advanced disease. Inhibitors of histone deacetylase (HDACi) induce re-differentiation in tumor cells and thereby re-establish sensitivity towards apoptotic stimuli. HDACi are entering the clinical stage of tumor treatment, and several substances are currently being tested in clinical trials to prove their efficacy in the treatment of leukemias and solid tumors. In this study, we investigated the impact of the HDACi valproic acid (VA) on TRAIL- and CD95-mediated apoptosis in hepatoma cells, as well as its sensitizing effect on a chemotherapeutic agent. Treatment of HepG2 cells with VA increased…

Cancer ResearchProgrammed cell deathCarcinoma Hepatocellularmedicine.medical_treatmentCellCASP8 and FADD-Like Apoptosis Regulating ProteinDown-RegulationCaspase 3ApoptosisBiologyReceptors Tumor Necrosis FactorTNF-Related Apoptosis-Inducing LigandAntineoplastic Combined Chemotherapy ProtocolsmedicineHumansfas ReceptorEpirubicinChemotherapyMembrane GlycoproteinsCaspase 3Tumor Necrosis Factor-alphaValproic AcidLiver NeoplasmsIntracellular Signaling Peptides and ProteinsGeneral MedicineCell cycleFas receptorHistone Deacetylase Inhibitorsmedicine.anatomical_structureOncologyApoptosisDrug Resistance NeoplasmCaspasesCancer researchHistone deacetylaseApoptosis Regulatory Proteins
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Apoptosis and the liver

2000

Regulation of the homeostatic balance between cell proliferation and programmed cell death, apoptosis, is essential for development and maintenance of multicellular organisms. Apoptosis is a genetically and evolutionarily highly conserved process. Analysis of the molecular mechanisms of apoptosis has led to a better understanding of many human diseases. Notably in cancer, but also in infectious or autoimmune disease, a deficiency in apoptosis is one of the key events in pathophysiology. On the other hand, overefficient apoptosis, as observed in fulminant liver failure, may be equally harmful for the organism indicating that a tight regulation of the apoptotic machinery is essential for surv…

Cancer ResearchProgrammed cell deathCeramideHepatitis Viral HumanDNA damageCellGenes mycApoptosisBiologyReceptors Tumor Necrosis Factorchemistry.chemical_compoundmedicineHumansfas ReceptorLiver DiseasesLiver NeoplasmsIntrinsic apoptosisGenes p53Genes bcl-2Liver TransplantationCell biologymedicine.anatomical_structureLiverchemistryUVB-induced apoptosisApoptosisImmunologyPoly(ADP-ribose) PolymerasesSignal transductionReceptors Transforming Growth Factor betaSeminars in Cancer Biology
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Targeting apoptosis proteins in hematological malignancies

2010

The apoptotic machinery plays a key role in hematopoietic cell homeostasis. Terminally differentiated cells are eliminated, at least in part, by apoptosis, whereas part of the apoptotic machinery, including one or several caspases, is required to go through very specific steps of the differentiation pathways. A number of hematological diseases involve a deregulation of this machinery, which in most cases is a decrease in cell sensitivity to pro-apoptotic signals through over-expression of anti-apoptotic molecules. In some situations however, e.g. in the erythroid lineage of low grade myelodysplastic syndromes, cell sensitivity to apoptosis is increased in a death receptor-dependent manner a…

Cancer ResearchProgrammed cell deathFas Ligand ProteinMyeloidCellular differentiationAmino Acid MotifsAntineoplastic AgentsApoptosisLigandsInhibitor of apoptosisTNF-Related Apoptosis-Inducing LigandCell Line TumormedicineHumansReceptorCaspasebiologyIntrinsic apoptosisCell DifferentiationCell biologyGene Expression Regulation Neoplasticmedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2OncologyApoptosisHematologic Neoplasmsbiology.proteinDrug Screening Assays AntitumorApoptosis Regulatory ProteinsSignal TransductionCancer Letters
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JNK and AP-1 mediate apoptosis induced by bortezomib in HepG2 cells via FasL/caspase-8 and mitochondria-dependent pathways

2006

The proteasome inhibitor bortezomib is an efficacious apoptotic agent in many tumor cells. This paper shows that bortezomib induced apoptosis in human hepatoma HepG2 cells associated with many modifications in the expression of survival or death factors. Although bortezomib increased the level of the protective factors HSP70 and HSP27, the effects of the drug that favour cell death were predominant. These events include accumulation of c-Jun, phospho-c-Jun and p53; increase in FasL level with activation of caspase-8; changes related to members of Bcl-2 family with increase in the level of pro-apoptotic members and decrease in that of anti-apoptotic ones; dissipation of mitochondrial potenti…

Cancer ResearchProgrammed cell deathFas Ligand ProteinProto-Oncogene Proteins c-junClinical BiochemistryPharmaceutical ScienceAntineoplastic AgentsApoptosisCaspase 8Cell LineBortezomibHsp27Cell Line TumormedicineHumansMitogen-Activated Protein Kinase 8Protease InhibitorsAP1Heat-Shock ProteinsPharmacologyCaspase 8Membrane GlycoproteinsbiologyJNK.Bortezomibc-JunLiver NeoplasmsBiochemistry (medical)c-junhepatomaCell BiologyapoptosiBoronic AcidsMitochondriaCell biologyTranscription Factor AP-1AP-1 transcription factorLiverProto-Oncogene Proteins c-bcl-2ApoptosisCaspasesPyrazinesTumor Necrosis Factorsbiology.proteinCancer researchProteasome inhibitorSignal Transductionmedicine.drugApoptosis
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