Search results for " CD"

showing 10 items of 587 documents

CD90+ liver cancer cells modulate endothelial cell phenotype through the release of exosomes containing H19 lncRNA

2015

Background CD90+ liver cancer cells have been described as cancer stem-cell-like (CSC), displaying aggressive and metastatic phenotype. Using two different in vitro models, already described as CD90+ liver cancer stem cells, our aim was to study their interaction with endothelial cells mediated by the release of exosomes. Methods Exosomes were isolated and characterized from both liver CD90+ cells and hepatoma cell lines. Endothelial cells were treated with exosomes, as well as transfected with a plasmid containing the full length sequence of the long non-coding RNA (lncRNA) H19. Molecular and functional analyses were done to characterize the endothelial phenotype after treatments. Results …

Cancer ResearchAngiogenesisAngiogenesis; CD90+ liver cancer cells; Exosomes; Long-non-coding RNA H19; Antigens Thy-1; Cell Adhesion; Cell Line Tumor; Endothelial Cells; Exosomes; Human Umbilical Vein Endothelial Cells; Humans; Liver Neoplasms; RNA Long Noncoding; Phenotype; Molecular Medicine; Oncology; Cancer ResearchBiologyCD90+ liver cancer cellsExosomesCell LineSettore BIO/13 - Biologia ApplicataCancer stem cellCell Line TumormedicineCell AdhesionHuman Umbilical Vein Endothelial CellsHumansCD90AntigensThy-1TumorExosomes Long-non-coding RNA H19 CD90+ liver cancer cells AngiogenesisResearchLiver NeoplasmsCancerEndothelial Cellsmedicine.diseaseMicrovesiclesCell biologyEndothelial stem cellPhenotypeOncologyembryonic structuresThy-1 AntigensRNAMolecular MedicineRNA Long NoncodingLong NoncodingAngiogenesisStem cellLiver cancerLong-non-coding RNA H19Molecular Cancer
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Role of exosomes released by chronic myelogenous leukemia cells in angiogenesis

2012

The present study is designed to assess if exosomes released from Chronic Myelogenous Leukemia (CML) cells may modulate angiogenesis. We have isolated and characterized the exosomes generated from LAMA84 CML cells and demonstrated that addition of exosomes to human vascular endothelial cells (HUVEC) induces an increase of both ICAM-1 and VCAM-1 cell adhesion molecules and interleukin-8 expression. The stimulation of cell-cell adhesion molecules was paralleled by a dose-dependent increase of adhesion of CML cells to a HUVEC monolayer. We further showed that the treatment with exosomes from CML cells caused an increase in endothelial cell motility accompanied by a loss of VE-cadherin and β-ca…

Cancer ResearchAngiogenesisVascular Cell Adhesion Molecule-1BiologyExosomesArticleExosomes Chronic Myelogenous Leukemia Cells Endothelial cells Tumor MicroenvironmentMiceAntigens CDCell Movementhemic and lymphatic diseasesCell Line TumorLeukemia Myelogenous Chronic BCR-ABL PositivemedicineCell AdhesionHuman Umbilical Vein Endothelial CellsTumor MicroenvironmentAnimalsHumansCell adhesionbeta CateninMatrigelTumor microenvironmentNeovascularization PathologicCell adhesion moleculeInterleukin-8medicine.diseaseCadherinsIntercellular Adhesion Molecule-1MicrovesiclesCell biologyEndothelial stem cellDrug CombinationsOncologyGene Expression RegulationCancer researchProteoglycansCollagenLamininChronic myelogenous leukemia
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Crosstalk between leukemia-associated proteins MOZ and MLL regulates HOX gene expression in human cord blood CD34+ cells

2010

MOZ and MLL, encoding a histone acetyltransferase (HAT) and a histone methyltransferase, respectively, are targets for recurrent chromosomal translocations found in acute myeloblastic or lymphoblastic leukemia. In MOZ (MOnocytic leukemia Zinc-finger protein)/CBP- or mixed lineage leukemia (MLL)-rearranged leukemias, abnormal levels of HOX transcription factors have been found to be critical for leukemogenesis. We show that MOZ and MLL cooperate to regulate these key genes in human cord blood CD34+ cells. These chromatin-modifying enzymes interact, colocalize and functionally cooperate, and both are recruited to multiple HOX promoters. We also found that WDR5, an adaptor protein essential fo…

Cancer ResearchAntigens CD34HistonesHistone H3hemic and lymphatic diseasesHistone methylationGeneticsHumansWDR5Tissue DistributionPromoter Regions GeneticHox geneneoplasmsMolecular BiologyCells CulturedHistone AcetyltransferasesHomeodomain ProteinsGeneticsBlood CellsbiologyIntracellular Signaling Peptides and ProteinsHistone-Lysine N-MethyltransferaseReceptor Cross-TalkU937 CellsHistone acetyltransferaseFetal BloodHematopoiesisCell biologyGene Expression RegulationHistone methyltransferasebiology.proteinMyeloid-Lymphoid Leukemia ProteinH3K4me3K562 CellsMyeloid-Lymphoid Leukemia ProteinProtein BindingOncogene
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Glioblastoma cells induce differential glutamatergic gene expressions in human tumor-associated microglia/macrophages and monocyte-derived macrophages

2015

Glioblastoma cells produce and release high amounts of glutamate into the extracellular milieu and subsequently can trigger seizure in patients. Tumor-associated microglia/macrophages (TAMs), consisting of both parenchymal microglia and monocytes-derived macrophages (MDMs) recruited from the blood, are known to populate up to 1/3 of the glioblastoma tumor environment and exhibit an alternative, tumor-promoting and supporting phenotype. However, it is unknown how TAMs respond to the excess extracellular glutamate in the glioblastoma microenvironment. We investigated the expressions of genes related to glutamate transport and metabolism in human TAMs freshly isolated from glioblastoma resecti…

Cancer ResearchAntigens Differentiation MyelomonocyticGlutamic AcidglutamateAMPA receptorSLC7A11Antigens CDTumor Cells CulturedExtracellularmedicineHumansReceptors AMPAGRIA2PharmacologyCD11b AntigenbiologyMicrogliaBrain NeoplasmsMacrophagesmonocyte-derived macrophagesCalcium-Binding ProteinsMicrofilament Proteinsglioblastomatumor-associated microglia/macrophagesGlutamate receptorSLC1A2Coculture TechniquesDNA-Binding ProteinsGlutaminemedicine.anatomical_structureGene Expression RegulationOncologyAstrocytesImmunologybiology.proteinCancer researchLeukocyte Common AntigensMolecular MedicineMicrogliaResearch PaperCancer Biology & Therapy
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The novel NF-κB inhibitor DHMEQ synergizes with celecoxib to exert antitumor effects on human liver cancer cells by a ROS-dependent mechanism

2012

In a previous work of ours dehydroxymethyl-epoxyquinomicin (DHMEQ), an inhibitor of NF-κB, was shown to induce apoptosis through Reactive Oxygen Species (ROS) production in hepatoma cells. The present study demonstrated that DHMEQ cooperates with Celecoxib (CLX) to decrease NF-κB DNA binding and to inhibit cell growth and proliferation more effectively than treatment with these single agents alone in the hepatoma cell lines HA22T/VGH and Huh-6. ROS production induced by the DHMEQ-CLX combination in turn generated the expression of genes involved in endoplasmic reticulum (ER) stress and silencing TRB3 mRNA significantly decreased DHMEQ-CLX-induced cell growth inhibition. Moreover, the DHMEQ-…

Cancer ResearchCarcinoma HepatocellularAntineoplastic AgentsApoptosisCell Cycle ProteinsProtein Serine-Threonine KinasesBiologyDHMEQ Celecoxib NF-jB CD95/CD95L Liver cancer cellsCell Line TumorSurvivinHumansGene silencingfas ReceptorProtein kinase BCell ProliferationSulfonamidesGene knockdownCyclooxygenase 2 InhibitorsCyclohexanonesCell growthEndoplasmic reticulumLiver NeoplasmsNF-kappa BDrug SynergismEndoplasmic Reticulum StressMolecular biologyAcetylcysteineRepressor ProteinsOncologyCelecoxibCell cultureApoptosisBenzamidesCancer researchPyrazolesPoly(ADP-ribose) PolymerasesReactive Oxygen SpeciesCancer Letters
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Dual regulation of SPI1/PU.1 transcription factor by heat shock factor 1 (HSF1) during macrophage differentiation of monocytes

2014

International audience; : In addition to their cytoprotective role in stressful conditions, heat shock proteins (HSPs) are involved in specific differentiation pathways, e.g. we have identified a role for HSP90 in macrophage differentiation of human peripheral blood monocytes exposed to Macrophage Colony-Stimulating Factor (M-CSF). Here, we show that deletion of the main transcription factor involved in heat shock gene regulation, heat shock factor 1 (HSF1), affects M-CSF-driven differentiation of mouse bone marrow cells. HSF1 transiently accumulates in the nucleus of human monocytes undergoing macrophage differentiation, including M-CSF-treated peripheral blood monocytes and phorbol ester-…

Cancer ResearchCellular differentiation[SDV]Life Sciences [q-bio][SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]Mice0302 clinical medicineHeat Shock Transcription FactorsHSF1[SDV.BDD]Life Sciences [q-bio]/Development BiologyCells CulturedComputingMilieux_MISCELLANEOUSRegulation of gene expression0303 health sciencesMice Inbred BALB C[SDV.MHEP.HEM]Life Sciences [q-bio]/Human health and pathology/HematologyHematology[SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry Molecular Biology/Biomolecules [q-bio.BM]3. Good healthDNA-Binding ProteinsOncology030220 oncology & carcinogenesismonocytesProteasome Endopeptidase ComplexAntigens Differentiation MyelomonocyticReceptors Cell Surface[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiology03 medical and health sciencesAntigens CDHeat shock proteinProto-Oncogene Proteinstranscription factorsAnimalsHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biology[ SDV.BDD ] Life Sciences [q-bio]/Development BiologyTranscription factor030304 developmental biologySPI1Macrophagesheat-shock proteinsfungi[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyMolecular biologyHsp70Heat shock factorMice Inbred C57BLcell differentiationGene Expression RegulationTrans-Activators[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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CD38/CD31, the CCL3 and CCL4 chemokines, and CD49d/vascular cell adhesion molecule-1 are interchained by sequential events sustaining chronic lymphoc…

2009

AbstractCD38 and CD49d are associated negative prognosticators in chronic lymphocytic leukemia (CLL). Despite evidence that both molecules are involved in interactions occurring between CLL and normal cells in the context of CLL-involved tissues, a functional link is still missing. Using gene expression profiles comparing CD38+CD49d+ versus CD38−CD49d− CLL cells, we showed overexpression of the CCL3 and CCL4 chemokines in cells from the former group. These chemokines were also up-regulated by CD38 signals in CLL; moreover, CCL3 was expressed by CLL cells from bone marrow biopsies (BMB) of CD38+CD49d+ but not CD38−CD49d− cases. High levels of CCR1 and, to a lesser extent, CCR5, the receptors…

Cancer ResearchChemokineChronic lymphocytic leukemiaIntegrin alpha4ApoptosisCD38immune system diseaseshemic and lymphatic diseasesReceptorsChronicMacrophages; Apoptosis; Membrane Glycoproteins; Humans; Integrin alpha4; Antigens CD38; Vascular Cell Adhesion Molecule-1; Endothelial Cells; Receptors Chemokine; Antigens CD31; Cell Survival; Bone Marrow Cells; Leukemia Lymphocytic Chronic B-Cell; Antigens CD; Up-Regulation; Chemokine CCL4; Chemokine CCL3; Cell LineChemokine CCL4Chemokine CCL3Membrane GlycoproteinsLeukemiaCell adhesion moleculehemic and immune systemsLymphocyticCDUp-RegulationPlatelet Endothelial Cell Adhesion Molecule-1Leukemiamedicine.anatomical_structureOncologyChemokineReceptors ChemokineTumor necrosis factor alphaStromal cellCell SurvivalVascular Cell Adhesion Molecule-1Bone Marrow CellsBiologyCell LineAntigens CDmedicineHumansAntigensMonocyteMacrophagesB-CellEndothelial Cellsmedicine.diseaseADP-ribosyl Cyclase 1Leukemia Lymphocytic Chronic B-CellCLL integrins chemokines CD49d CD38 prognosis.Cancer researchbiology.proteinCD31Settore MED/15 - Malattie del SangueCD38
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Optimization of retroviral-mediated gene transfer to human NOD/SCID mouse repopulating cord blood cells through a systematic analysis of protocol var…

1999

Abstract Retroviral transduction of human hematopoietic stem cells is still limited by lack of information about conditions that will maximize stem cell self-renewal divisions in vitro. To address this, we first compared the kinetics of entry into division of single human CD34 + CD38 − cord blood (CB) cells exposed in vitro to three different flt3-ligand (FL)-containing cytokine combinations. Of the three combinations tested, FL + hyperinterleukin 6 (HIL-6) yielded the least clones and these developed at a slow rate. With either FL + Steel factor (SF) + HIL-6 + thrombopoietin (TPO) or FL + SF + interleukin 3 (IL-3) + IL-6 + granulocyte-colony-stimulating factor (G-CSF), >90% of the cells th…

Cancer ResearchGenetic VectorsCD34Antigens CD34Stem cell factorMice SCIDCD38BiologyImmunophenotypingViral vectorMiceNAD+ NucleosidaseAntigens CDMice Inbred NODTransduction GeneticGeneticsAnimalsHumansADP-ribosyl CyclaseMolecular BiologyInterleukin 3Membrane GlycoproteinsGene Transfer TechniquesInfant NewbornMembrane ProteinsCell BiologyHematologyFetal BloodADP-ribosyl Cyclase 1Antigens DifferentiationVirologyMolecular biologyHaematopoiesisRetroviridaeCord bloodStem cellCell DivisionExperimental Hematology
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The AC133 epitope, but not the CD133 protein, is lost upon cancer stem cell differentiation.

2010

Abstract Colon cancer stem cells (CSC) can be identified with AC133, an antibody that detects an epitope on CD133. However, recent evidence suggests that expression of CD133 is not restricted to CSCs, but is also expressed on differentiated tumor cells. Intriguingly, we observed that detection of the AC133 epitope on the cell surface decreased upon differentiation of CSC in a manner that correlated with loss of clonogenicity. However, this event did not coincide with a change in CD133 promoter activity, mRNA, splice variant, protein expression, or even cell surface expression of CD133. In contrast, we noted that with CSC differentiation, a change occured in CD133 glycosylation. Thus, AC133 …

Cancer ResearchGlycosylationGlycosylationCellular differentiationCellAC 133 EpitopeDown-RegulationMice SCIDEpitopechemistry.chemical_compoundEpitopesMiceCancer stem cellAntigens CDMice Inbred NODProminin-1medicineTumor Cells CulturedAnimalsHumansProtein IsoformsAC133 AntigenRNA MessengerPromoter Regions GeneticneoplasmsGlycoproteinsbiologyCell DifferentiationMolecular biologycarbohydrates (lipids)Gene Expression Regulation Neoplasticmedicine.anatomical_structureOncologychemistryembryonic structuresColonic Neoplasmsbiology.proteinNeoplastic Stem CellsAntibodyStem cellPeptidesCancer research
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In vitro and in vivo purging of B lymphoma cells from stem-cell products using anti-CD20 Abs.

2000

Background Autologous stem-cell transplantation has proved curative therapy for relapsed NHL. However, recurrence of underlying disease remains the major cause of treatment failure in this setting. Methods Development of effective MAb therapy directed against the B cell surface antigen CD20 has added a valuable tool of clearing contaminating lymphoma cells from stem-cell products by either in vitro or in vivo application. Results Transplantation of successfully in vitro purged bone marrow using Mabs has been correlated with prolonged survival in large Phase-II study. So far, no randomized trial could demonstrate a therapeutic benefit for in vitro purging. The anti-CD20 Mab rituximab has bee…

Cancer ResearchLymphoma B-CellNeoplasm ResidualImmunologyAntineoplastic AgentsCell SeparationAntibodies Monoclonal Murine-DerivedClinical Trials Phase II as Topicimmune system diseaseshemic and lymphatic diseasesmedicineImmunology and AllergyHumansGenetics (clinical)B cellCD20Transplantationbiologybusiness.industryStem CellsBone Marrow PurgingAntibodies MonoclonalCell Biologymedicine.diseaseAntigens CD20LymphomaTransplantationHaematopoiesismedicine.anatomical_structureOncologyImmunologybiology.proteinRituximabBone marrowStem cellbusinessRituximabmedicine.drugStem Cell TransplantationCytotherapy
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