Search results for " Cell Line"

showing 10 items of 238 documents

IL4 Primes the Dynamics of Breast Cancer Progression via DUSP4 Inhibition

2017

Abstract The tumor microenvironment supplies proinflammatory cytokines favoring a permissive milieu for cancer cell growth and invasive behavior. Here we show how breast cancer progression is facilitated by IL4 secreted by adipose tissue and estrogen receptor–positive and triple-negative breast cancer cell types. Blocking autocrine and paracrine IL4 signaling with the IL4Rα antagonist IL4DM compromised breast cancer cell proliferation, invasion, and tumor growth by downregulating MAPK pathway activity. IL4DM reduced numbers of CD44+/CD24− cancer stem-like cells and elevated expression of the dual specificity phosphatase DUSP4 by inhibiting NF-κB. Enforced expression of DUSP4 drove conversio…

0301 basic medicineCancer ResearchBlotting WesternCA 15-3Breast Neoplasms03 medical and health sciencesParacrine signalling0302 clinical medicineBreast cancerCell Line TumorTumor MicroenvironmentmedicineHumansskin and connective tissue diseasesAutocrine signallingDual-Specificity PhosphataseBlotting Western; Breast Neoplasms; Cell Line Tumor; Disease Progression; Dual-Specificity Phosphatases; Female; Flow Cytometry; Heterografts; Humans; Interleukin-4; Mitogen-Activated Protein Kinase Phosphatases; Tumor Microenvironment; Oncology; Cancer ResearchTumor microenvironmentbiologyCD44CancerFlow Cytometrymedicine.disease030104 developmental biologyOncology030220 oncology & carcinogenesisImmunologyCancer cellDisease Progressionbiology.proteinCancer researchDual-Specificity PhosphatasesHeterograftsMitogen-Activated Protein Kinase PhosphatasesFemaleInterleukin-4HeterograftMitogen-Activated Protein Kinase PhosphataseBreast NeoplasmHumanCancer Research
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Establishment and characterization of a highly immunogenic human renal carcinoma cell line.

2015

Renal cell carcinoma (RCC) is the most common kidney cancer, and accounts for ~3% of all adult malignancies. RCC has proven refractory to conventional treatment modalities but appears to be the only histological form that shows any consistent response to immunotherapeutic approaches. The development of a clinically effective vaccine remains a major strategic target for devising active specific immunotherapy in RCC. We aimed to identify a highly immunogenic antigenic format for immunotherapeutic approaches, so as to boost immune responses in RCC patients. We established and cloned an immunogenic cell line, RCC85#21 named Elthem, which was derived from a non-aggressive and non-metastatic clea…

0301 basic medicineCancer ResearchCellClone (cell biology)BiologyImmunophenotyping03 medical and health sciencesimmunogenic antigenic format0302 clinical medicineImmune systemAntigenAntigens NeoplasmCell Line TumormedicineCytotoxic T cellHumansElectrophoresis Gel Two-DimensionalCarcinoma Renal Cellrenal cancer cell lineSystems BiologyArticlesCell cycleMolecular biologyKidney Neoplasms030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisSpectrometry Mass Matrix-Assisted Laser Desorption-Ionizationcell proteomeClear cell carcinomaK562 CellsCD8International journal of oncology
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Extracellular Vesicles Shed by Melanoma Cells Contain a Modified Form of H1.0 Linker Histone and H1.0 mRNA-binding Proteins

2016

Extracellular vesicles (EVs) are shed in the extracellular environment by both prokaryotes and eukaryotes. Although produced from both normal and cancer cells, malignant cells release a much higher amount of EVs, which also contain tumor-specific proteins and RNAs. We previously found that G26/24 oligodendroglioma cells shed EVs that contain the pro-apoptotic factors FasL and TRAIL1-2. Interestingly, G26/24 release, via EVs, extracellular matrix remodelling proteases3, and H1° histone protein4, and mRNA. To shed further light on the role of EVs in discarding proteins and mRNAs otherwise able to counteract proliferative signals, we studied a melanoma cell line (A375). We found that also thes…

0301 basic medicineCancer ResearchCellular differentiationBlotting WesternFluorescent Antibody TechniqueMYEF2ApoptosisRNA-binding proteinexosomesmembrane vesiclesReal-Time Polymerase Chain ReactionChromatography AffinityHistones03 medical and health sciencesH1.0 linker histone; RNA-binding proteins (RBPs); extracellular vesicles (EVs) membrane vesicles (MVs); exosomes; MYEF2Settore BIO/10 - BiochimicaTumor Cells CulturedHumansexosomeSecretionRNA MessengerSettore BIO/06 - Anatomia Comparata E Citologiamelanoma cell line (A375) myelin expression factor-2 (MYEF2)MelanomaTranscription factorCell ProliferationH1.0 linker histonebiologyReverse Transcriptase Polymerase Chain ReactionEXTRACELLULAR VESICLESRNA-Binding ProteinsRNACell DifferentiationArticlesCell biologyBlotCell Transformation Neoplastic030104 developmental biologyHistoneOncologySpectrometry Mass Matrix-Assisted Laser Desorption-IonizationCancer cellbiology.proteinRNA-binding proteins (RBPs)extracellular vesicles (EVs) membrane vesicles (MVs)
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Oxidative stress preconditioning of mouse perivascular myogenic progenitors selects a subpopulation of cells with a distinct survival advantage in vi…

2018

AbstractCell engraftment, survival and integration during transplantation procedures represent the crux of cell-based therapies. Thus, there have been many studies focused on improving cell viability upon implantation. We used severe oxidative stress to select for a mouse mesoangioblast subpopulation in vitro and found that this subpopulation retained self-renewal and myogenic differentiation capacities while notably enhancing cell survival, proliferation and migration relative to unselected cells. Additionally, this subpopulation of cells presented different resistance and recovery properties upon oxidative stress treatment, demonstrating select advantages over parental mesoangioblasts in …

0301 basic medicineCancer ResearchCellular differentiationCellstem cells; oxidative stress; clone isolation/dk/atira/pure/subjectarea/asjc/2800/2804Mice SCIDp38 Mitogen-Activated Protein KinasesMiceCell MovementProtein IsoformsMuscular Dystrophy/dk/atira/pure/subjectarea/asjc/2400/2403Settore BIO/06 - Anatomia Comparata E Citologiaeducation.field_of_studylcsh:CytologyStem CellsSettore BIO/13Cell DifferentiationSkeletalCell biologymedicine.anatomical_structureMuscleMatrix Metalloproteinase 2Animals; Cell Cycle Checkpoints; Cell Differentiation; Cell Line; Cell Movement; Cell Survival; Hydrogen Peroxide; Matrix Metalloproteinase 2; Mice; Mice SCID; Muscle Skeletal; Muscular Dystrophy Animal; Oxidative Stress; Protein Isoforms; Reactive Oxygen Species; Sarcoglycans; Stem Cell Transplantation; Stem Cells; p38 Mitogen-Activated Protein Kinases/dk/atira/pure/subjectarea/asjc/1300/1306/dk/atira/pure/subjectarea/asjc/1300/1307Cell SurvivalPopulationImmunologyBiologySCIDArticleCell Line03 medical and health sciencesCellular and Molecular NeuroscienceIn vivoSarcoglycansmedicineAnimalsProgenitor celllcsh:QH573-671educationMuscle Skeletaloxidative streMesoangioblastAnimalCell BiologyCell Cycle CheckpointsHydrogen PeroxideMuscular Dystrophy Animalclone isolationTransplantationstem cellOxidative Stress030104 developmental biologyCell cultureReactive Oxygen SpeciesStem Cell TransplantationCell Death & Disease
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The phospholipase DDHD1 as a new target in colorectal cancer therapy

2018

Background Our previous study demonstrates that Citrus-limon derived nanovesicles are able to decrease colon cancer cell viability, and that this effect is associated with the downregulation of the intracellular phospholipase DDHD domain-containing protein 1 (DDHD1). While few studies are currently available on the contribution of DDHD1 in neurological disorders, there is no information on its role in cancer. This study investigates the role of DDHD1 in colon cancer. Methods DDHD1 siRNAs and an overexpression vector were transfected into colorectal cancer and normal cells to downregulate or upregulate DDHD1 expression. In vitro and in vivo assays were performed to investigate the functional…

0301 basic medicineCancer ResearchColorectal cancerApoptosisMiceSettore BIO/13 - Biologia ApplicataGene Regulatory NetworksMolecular Targeted TherapyCitrus-limon nanovesicleTransfectionlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens3. Good healthCitrus-limon nanovesicles; Colorectal cancer; Phospholipase DDHD1; Oncology; Cancer ResearchOncologyPhospholipasesCitrus-limon nanovesicles; Colorectal cancer; Phospholipase DDHD1; Animals; Antineoplastic Agents; Apoptosis; Cell Line Tumor; Cell Proliferation; Colorectal Neoplasms; Computational Biology; Disease Models Animal; Female; Gene Expression Profiling; Gene Ontology; Gene Regulatory Networks; Gene Silencing; Humans; MAP Kinase Signaling System; Mice; Phospholipases; Signal Transduction; Xenograft Model Antitumor Assays; Biomarkers Tumor; Molecular Targeted TherapyFemaleColorectal NeoplasmsSignal TransductionMAP Kinase Signaling SystemAntineoplastic Agentslcsh:RC254-282Citrus-limon nanovesicles03 medical and health sciencesDownregulation and upregulationIn vivoCell Line TumorBiomarkers TumormedicineAnimalsHumansGene silencingGene SilencingPhospholipase DDHD1Cell Proliferationbusiness.industryCell growthGene Expression ProfilingResearchComputational BiologyCancermedicine.diseaseXenograft Model Antitumor AssaysColorectal cancerDisease Models AnimalGene Ontology030104 developmental biologyApoptosisCancer researchbusiness
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A receptor-antibody hybrid hampering MET-driven metastatic spread

2021

AbstractBackgroundThe receptor encoded by the MET oncogene and its ligand Hepatocyte Growth Factor (HGF) are at the core of the invasive-metastatic behavior. In a number of instances genetic alterations result in ligand-independent onset of malignancy (METaddiction). More frequently, ligand stimulation of wild-type MET contributes to progression toward metastasis (METexpedience). Thus, while MET inhibitors alone are effective in the first case, combination therapy with ligand inhibitors is required in the second condition.MethodsIn this paper, we generated hybrid molecules gathering HGF and MET inhibitory properties. This has been achieved by ‘head-to-tail’ or ‘tail-to-head’ fusion of a sin…

0301 basic medicineCancer ResearchImmunoconjugatesmedicine.medical_treatmentMice SCIDEpitopeFusion proteins; HGF; MET; Metastasis; Targeted therapy; A549 Cells; Animals; Binding Sites Antibody; Cell Line Tumor; Cell Proliferation; Female; Hepatocyte Growth Factor; Humans; Immunoconjugates; Immunoglobulin Fab Fragments; Mice; Mice SCID; Neoplasm Metastasis; Neoplasms; Proto-Oncogene Proteins c-met; Rats; Rats Sprague-Dawley; Recombinant Proteins; Xenograft Model Antitumor AssaysMetastasisTargeted therapyMetastasisRats Sprague-DawleyTargeted therapyMice0302 clinical medicineNeoplasmsHGFNeoplasm MetastasisReceptorTumorHepatocyte Growth FactorChemistryProto-Oncogene Proteins c-metlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensRecombinant ProteinsOncology030220 oncology & carcinogenesisMETFemaleHepatocyte growth factormedicine.drugSCIDlcsh:RC254-282Cell LineImmunoglobulin Fab Fragments03 medical and health sciencesCell Line TumorPancreatic cancermedicineAnimalsHumansAntibodyCell ProliferationBinding SitesResearchmedicine.diseaseXenograft Model Antitumor AssaysFusion proteinRatsFusion proteins030104 developmental biologyA549 CellsCancer cellCancer researchBinding Sites AntibodySprague-DawleyJournal of Experimental & Clinical Cancer Research
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Imiquimod inhibits growth and induces differentiation of myeloid leukemia cell lines

2018

Background: The antitumoral effects of different Toll-like receptor (TLRs) agonists is mediated by activating immune responses to suppress tumors growth, although TLR ligands may also have a direct effect on tumoral cells. Given that TLR signaling induces hematopoietic cell differentiations this may serve as a novel differentiation therapeutic approach for AML. Methods: We investigated the effects of agonists for the ten human TLRs on the proliferation, apoptosis, cell cycle and differentiation of ten different types of myeloid leukemia cell lines (HL-60, U-937, KG-1, KG-1a, K-562, Kasumi-1, EOL-1, NB4, MOLM-13 and HEL). Proliferation was measured using the CellTiter 96 (R) Aqueous One Solu…

0301 basic medicineCancer ResearchMyeloidImiquimodlcsh:RC254-282Flow cytometry03 medical and health sciences0302 clinical medicineToll-like receptorGeneticsmedicineCytotoxic T cellMyeloid leukemia cell lineslcsh:QH573-671Toll-like receptorImiquimodmedicine.diagnostic_testChemistryCell growthlcsh:CytologyMyeloid leukemiaCell cyclelcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisCancer researchPrimary Researchmedicine.drugCancer Cell International
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Targeting COPZ1 non-oncogene addiction counteracts the viability of thyroid tumor cells

2017

Abstract Thyroid carcinoma is generally associated with good prognosis, but no effective treatments are currently available for aggressive forms not cured by standard therapy. To find novel therapeutic targets for this tumor type, we had previously performed a siRNA-based functional screening to identify genes essential for sustaining the oncogenic phenotype of thyroid tumor cells, but not required to the same extent for the viability of normal cells (non-oncogene addiction paradigm). Among those, we found the coatomer protein complex ζ1 (COPZ1) gene, which is involved in intracellular traffic, autophagy and lipid homeostasis. In this paper, we investigated the mechanisms through which COPZ…

0301 basic medicineCancer ResearchTime FactorsCOPZ1ApoptosisCOPZ1Thyroid cancerThyroid NeoplasmThyroidRNAi TherapeuticCell death; COPZ1; Non-oncogene addiction; Thyroid carcinoma; Animals; Apoptosis; Autophagy; Cell Line Tumor; Cell Survival; Coatomer Protein; Endoplasmic Reticulum Stress; Female; Gene Expression Regulation Neoplastic; Humans; Mice Nude; RNA Interference; Signal Transduction; Thyroid Neoplasms; Time Factors; Transfection; Tumor Burden; Unfolded Protein Response; Xenograft Model Antitumor Assays; RNAi Therapeutics; Oncology; Cancer ResearchEndoplasmic Reticulum StressOncogene AddictionTumor BurdenGene Expression Regulation Neoplasticmedicine.anatomical_structureOncologyFemaleRNA InterferenceNon-oncogene addictionHumanSignal TransductionCell deathProgrammed cell deathXenograft Model Antitumor AssayTime FactorCell SurvivalMice NudeBiologyTransfectionCoatomer ProteinThyroid carcinomaThyroid carcinoma03 medical and health sciencesCell Line TumorAutophagymedicineAnimalsHumansThyroid NeoplasmsEndoplasmic Reticulum StreAnimalAutophagyApoptosimedicine.diseaseXenograft Model Antitumor AssaysRNAi Therapeutics030104 developmental biologyImmunologyUnfolded Protein ResponseCancer researchUnfolded protein response
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A Set of Cell Lines Derived from a Genetic Murine Glioblastoma Model Recapitulates Molecular and Morphological Characteristics of Human Tumors

2021

Simple Summary Glioblastoma (GBM) is a highly aggressive and almost inevitably lethal brain tumor. Animal models for GBM are crucial to study how the tumor evolves in vivo and to test novel treatment options. Most currently available models are based on the transplantation of human GBM cells into mice with a defective immune system. However, this approach does not allow to study the contribution of immune cells to GBM growth and to test immunotherapies. Transplantation of murine GBM cells overcomes this limitation, however, up to now, only a limited number, which mostly do not mimic important characteristics of human GBM, have been available. Via in vivo passaging, we established a set of m…

0301 basic medicineCancer Researchmouse modelCentral nervous systemBrain tumorBiologylcsh:RC254-282GenomeArticleTranscriptome03 medical and health sciences0302 clinical medicineIn vivoGliomamedicinePTENsyngeneic cell lineglioblastomalcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseasenervous system diseases030104 developmental biologymedicine.anatomical_structureOncologyCell culture030220 oncology & carcinogenesisCancer researchbiology.proteinCancers
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Design, synthesis, and biological evaluation of a new class of benzo[b]furan derivatives as antiproliferative agents, with in silico predicted antitu…

2018

A new series of 3-benzoylamino-5-(1H-imidazol-4-yl)methylaminobenzo[b]furans were synthesized and screened as antitumor agents. As a general trend, tested compounds showed concentration-dependent antiproliferative activity against HeLa and MCF-7 cancer cell lines, exhibiting GI50 values in the low micromolar range. In most cases, insertion of a methyl substituent on the imidazole moiety improved the antiproliferative activity. Therefore, methyl-imidazolyl-benzo[b]furans compounds were tested in cell cycle perturbation experiments, producing cell cycle arrest with proapoptotic effects. Their core similarity to known colchicine binding site binders led us to further study the structure featur…

0301 basic medicineCell cycle checkpointinduced fit docking studieantitubulin agents01 natural sciencesBiochemistryHeLa and MCF-7 cell linesHeLachemistry.chemical_compoundTubulinFuranDrug DiscoveryImidazoleMoietybiologyHeLa and MCF-7 cell lineG2/M phaseTubulin ModulatorsMolecular Docking SimulationAntiproliferative AgentsMCF-7 CellsMolecular MedicineVLAK protocolantitubulin agentStereochemistryIn silicoSubstituent3-benzoylamino-5-(1H-imidazol-4-yl)methylaminobenzo[b]furansAntineoplastic Agentsinduced fit docking studiesantitumor agents03 medical and health sciencesHumanscolchicine binding siteBenzofuransCell ProliferationPharmacologyBinding Sites010405 organic chemistryOrganic ChemistryCell Cycle Checkpoints3-benzoylamino-5-(1H-imidazol-4-yl)methylaminobenzo[b]furanbiology.organism_classification0104 chemical sciencesProtein Structure Tertiary030104 developmental biologychemistryantitumor agentDrug DesignColchicineHeLa Cells
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