Search results for "Line"

showing 10 items of 31271 documents

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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AP2α controls the dynamic balance between miR-126&126* and miR-221&222 during melanoma progression

2016

Accumulating evidences have shown the association between aberrantly expressed microRNAs (miRs) and cancer, where these small regulatory RNAs appear to dictate the cell fate by regulating all the main biological processes. We demonstrated the responsibility of the circuitry connecting the oncomiR-221&222 with the tumor suppressors miR-126&126∗ in melanoma development and progression. According to the inverse correlation between endogenous miR-221&222 and miR-126&126∗, respectively increasing or decreasing with malignancy, their enforced expression or silencing was sufficient for a reciprocal regulation. In line with the opposite roles of these miRs, protein analyses confirmed the reverse ex…

0301 basic medicineCancer ResearchCellular differentiationSettore MED/08 - Anatomia Patologicagrowth-factorCell fate determinationBiologyFatty Acid-Binding ProteinsBioinformaticsap-2 transcription factorlaw.inventioncutaneous melanoma03 medical and health sciencesMolecular Biology; Cancer Research; Genetics0302 clinical medicinelawTranscription (biology)Cell Line TumormicroRNAGeneticsmedicineHumansGene silencingMelanomaMolecular BiologyPsychological repressionsquamous-cell carcinoma; ap-2 transcription factor; cutaneous melanoma; growth-factor; metastatic melanoma; terminal fragment; cancer-cells; tumor-growth; mir-126; methylationMelanomaCell Differentiationsquamous-cell carcinomatumor-growthmedicine.diseaseMicroRNAscancer-cells030104 developmental biologyterminal fragmentmir-126030220 oncology & carcinogenesisDisease ProgressionCancer researchSuppressorOriginal Articlemethylationmetastatic melanomaOncogene
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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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Targeting chemoresistant colorectal cancer via systemic administration of a BMP7 variant

2020

Abstract Despite intense research and clinical efforts, patients affected by advanced colorectal cancer (CRC) have still a poor prognosis. The discovery of colorectal (CR) cancer stem cell (CSC) as the cell compartment responsible for tumor initiation and propagation may provide new opportunities for the development of new therapeutic strategies. Given the reduced sensitivity of CR-CSCs to chemotherapy and the ability of bone morphogenetic proteins (BMP) to promote colonic stem cell differentiation, we aimed to investigate whether an enhanced variant of BMP7 (BMP7v) could sensitize to chemotherapy-resistant CRC cells and tumors. Thirty-five primary human cultures enriched in CR-CSCs, includ…

0301 basic medicineCancer ResearchColorectal cancerBone Morphogenetic Protein 7Cellular differentiationCellAntineoplastic AgentsTumor initiationBiologyArticleMice03 medical and health sciences0302 clinical medicineSettore MED/04 - PATOLOGIA GENERALECancer stem cellCell Line TumorGeneticsmedicineAnimalsHumansbmp7Molecular BiologyPI3K/AKT/mTOR pathwayPhosphoinositide-3 Kinase InhibitorsCancer stem cellsMesenchymal stem cellWnt signaling pathwayCell Differentiationmedicine.diseasecolorectal cancer bmp7Colorectal cancerXenograft Model Antitumor Assays030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisMutationNeoplastic Stem CellsCancer researchColorectal NeoplasmsOncogene
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Knockdown of hnRNPK leads to increased DNA damage after irradiation and reduces survival of tumor cells.

2017

Radiotherapy is an important treatment option in the therapy of multiple tumor entities among them head and neck squamous cell carcinoma (HNSCC). However, the success of radiotherapy is limited by the development of radiation resistances. Heterogeneous nuclear ribonucleoprotein K (hnRNPK) is a cofactor of p53 and represents a potential target for radio sensitization of tumor cells. In this study, we analyzed the impact of hnRNPK on the DNA damage response after gamma irradiation. By yH2AX foci analysis, we found that hnRNPK knockdown increases DNA damage levels in irradiated cells. Tumor cells bearing a p53 mutation showed increased damage levels and delayed repair. Knockdown of hnRNPK appl…

0301 basic medicineCancer ResearchDNA damageCell Survivalmedicine.medical_treatmentmedicine.disease_causeRadiation ToleranceHeterogeneous-Nuclear Ribonucleoprotein KHistones03 medical and health sciences0302 clinical medicineCell Line TumormedicineCarcinomaGene Knockdown TechniquesHumansMutationGene knockdownChemistrySquamous Cell Carcinoma of Head and NeckStem CellsGeneral Medicinemedicine.diseaseHead and neck squamous-cell carcinomaRadiation therapy030104 developmental biologyCell cultureHead and Neck Neoplasms030220 oncology & carcinogenesisGene Knockdown TechniquesCancer researchCarcinoma Squamous CellTumor Suppressor Protein p53DNA DamageCarcinogenesis
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Targeting prohibitins with chemical ligands inhibits KRAS-mediated lung tumours.

2017

KRAS is one of the most frequently mutated oncogenes in human non-small cell lung cancers (NSCLCs). RAS proteins trigger multiple effector signalling pathways including the highly conserved RAF-MAPK pathway. CRAF, a direct RAS effector protein, is required for KRAS-mediated tumourigenesis. Thus, the molecular mechanisms driving the activation of CRAF are intensively studied. Prohibitin 1 (PHB1) is an evolutionarily conserved adaptor protein and interaction of CRAF with PHB1 at the plasma membrane is essential for CRAF activation. Here, we demonstrate that PHB1 is highly expressed in NSCLC patients and correlates with poor survival. Targeting of PHB1 with two chemical ligands (rocaglamide an…

0301 basic medicineCancer ResearchEGF Family of ProteinsLung NeoplasmsBiologyLigandsProto-Oncogene Proteins p21(ras)03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineGrowth factor receptorRocaglamideEpidermal growth factorCarcinoma Non-Small-Cell LungCell Line TumorProhibitinsGeneticsAnimalsHumansMolecular Targeted TherapyProhibitinMolecular BiologyBenzofuransCell ProliferationRas InhibitorMice KnockoutTNF Receptor-Associated Factor 3EffectorXenograft Model Antitumor Assaysrespiratory tract diseasesCell biologyProto-Oncogene Proteins p21(ras)Gene Expression Regulation NeoplasticRepressor Proteins030104 developmental biologychemistry030220 oncology & carcinogenesisras Proteinsraf KinasesSignal transductionSignal TransductionOncogene
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PHD3 Controls Lung Cancer Metastasis and Resistance to EGFR Inhibitors through TGFα.

2018

Abstract Lung cancer is the leading cause of cancer-related death worldwide, in large part due to its high propensity to metastasize and to develop therapy resistance. Adaptive responses to hypoxia and epithelial–mesenchymal transition (EMT) are linked to tumor metastasis and drug resistance, but little is known about how oxygen sensing and EMT intersect to control these hallmarks of cancer. Here, we show that the oxygen sensor PHD3 links hypoxic signaling and EMT regulation in the lung tumor microenvironment. PHD3 was repressed by signals that induce EMT and acted as a negative regulator of EMT, metastasis, and therapeutic resistance. PHD3 depletion in tumors, which can be caused by the EM…

0301 basic medicineCancer ResearchEpithelial-Mesenchymal TransitionLung NeoplasmsMice NudeAntineoplastic AgentsSMADDrug resistanceMetastasisHypoxia-Inducible Factor-Proline DioxygenasesMitochondrial Proteins03 medical and health sciencesErlotinib HydrochlorideMice0302 clinical medicineDownregulation and upregulationCell Line TumorTumor MicroenvironmentMedicineAnimalsHumansNeoplasm MetastasisLung cancerProtein Kinase InhibitorsEGFR inhibitorsbusiness.industryIntracellular Signaling Peptides and ProteinsCancerTransforming Growth Factor alphamedicine.diseaseHCT116 CellsXenograft Model Antitumor AssaysCell HypoxiaErbB Receptors030104 developmental biologyOncologyA549 CellsDrug Resistance Neoplasm030220 oncology & carcinogenesisembryonic structuresCancer researchFemaleErlotinibbusinessApoptosis Regulatory Proteinsmedicine.drugCancer research
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Transcriptional profiling of circulating tumor cells in multiple myeloma: a new model to understand disease dissemination

2020

The reason why a few myeloma cells egress from the bone marrow (BM) into peripheral blood (PB) remains unknown. Here, we investigated molecular hallmarks of circulating tumor cells (CTCs) to identify the events leading to myeloma trafficking into the bloodstream. After using next-generation flow to isolate matched CTCs and BM tumor cells from 32 patients, we found high correlation in gene expression at single-cell and bulk levels (r ≥ 0.94, P = 10−16), with only 55 genes differentially expressed between CTCs and BM tumor cells. CTCs overexpressed genes involved in inflammation, hypoxia, or epithelial–mesenchymal transition, whereas genes related with proliferation were downregulated in CTCs…

0301 basic medicineCancer ResearchEpithelial-Mesenchymal TransitionTranscription GeneticGene ExpressionBiologycirculating tumor cell03 medical and health sciences0302 clinical medicineCirculating tumor cellBone MarrowCell MovementCancer stem cellCell Line TumorTumor MicroenvironmentmedicineHumansHypoxiaMultiple myelomaCell ProliferationInflammationGene knockdownliquid biopsyCD44CENPFHematologyNeoplastic Cells CirculatingPrognosismedicine.disease3. Good healthmultiple myeloma030104 developmental biologymedicine.anatomical_structureOncologyCell culture030220 oncology & carcinogenesisNeoplastic Stem CellsCancer researchbiology.proteinBone marrow
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