Search results for "Cell Line"

showing 10 items of 2924 documents

Polysialic acid chains exhibit enhanced affinity for ordered regions of membranes.

2018

Polysialic acid (polySia) forms linear chains which are usually attached to the external surface of the plasma membrane mainly through the Neural Cell Adhesion Molecule (NCAM) protein. It is exposed on neural cells, several types of cancer cells, dendritic cells, and egg and sperm cells. There are several lipid raft-related phenomena in which polySia is involved; however the mechanisms of polySia action as well as determinants of its localization in lipid raft microdomains are still unknown, although the majority of NCAM molecules in the liquid-ordered raft membrane fractions of neural cells appear to be polysialylated. Here we investigate the affinity of polySia (both soluble and NCAM-depe…

0301 basic medicineLipid BilayersBiophysicsPolysialic acidBiochemistryGiant vesicles03 medical and health sciencesNeuroblastomaRafts0302 clinical medicineMembrane MicrodomainsCell Line TumorNeuroblastoma cellsFluorescence Resonance Energy TransferHumansLipid raftNeuronsLiposomePolysialic acidChemistryCell MembraneCell BiologyRaftLipidsKinetics030104 developmental biologyMembraneFörster resonance energy transferMicroscopy FluorescenceSolubilityCancer cellLiposomesFRETBiophysicsSialic AcidsNeural cell adhesion molecule030217 neurology & neurosurgeryProtein BindingBiochimica et biophysica acta. Biomembranes
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Ceftaroline modulates the innate immune and host defense responses of immunocompetent cells exposed to cigarette smoke.

2017

Abstract Background Cigarette smoke, the principal risk factor for chronic obstructive pulmonary disease (COPD), negatively influences the effectiveness of the immune system’s response to a pathogen. The antibiotic ceftaroline exerts immune-modulatory effects in bronchial epithelial cells exposed to cigarette smoke. Aims and methods The present study aims to assess the effects of ceftaroline on TLR2 and TLR4 expression, LPS binding and TNF-α and human beta defensin (HBD2) release in an undifferentiated and PMA-differentiated human monocyte cell line (THP-1) exposed or not to cigarette smoke extracts (CSE). TLR2, TLR4, and LPS binding were assessed by flow cytometry, TNF-α and HBD2 release w…

0301 basic medicineLipopolysaccharidesbeta-DefensinsCell SurvivalCephalosporinLipopolysaccharideToxicologyMonocytes03 medical and health sciencesImmunologic Factor0302 clinical medicineImmune systemCell Line TumorSmokeAnti-Bacterial AgentmedicineHumansImmunologic FactorsInnate immune systemImmunocompetent cellDose-Response Relationship Drugbusiness.industryTumor Necrosis Factor-alphaMonocyteMacrophagesSmokingAntibioticCigarette smokeGeneral MedicineImmunity InnateToll-Like Receptor 2Anti-Bacterial AgentsCephalosporinsHost-Pathogen InteractionToll-Like Receptor 4TLR2030104 developmental biologymedicine.anatomical_structureBeta defensinCell cultureImmunologyHost-Pathogen InteractionsTLR4lipids (amino acids peptides and proteins)Tumor necrosis factor alphabusinessImmunocompetence030215 immunologyToxicology letters
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Protein tyrosine phosphatase 1b deficiency protects against hepatic fibrosis by modulating nadph oxidases

2019

Inflammation is typically associated with the development of fibrosis, cirrhosis and hepatocellular carcinoma. The key role of protein tyrosine phosphatase 1B (PTP1B) in inflammatory responses has focused this study in understanding its implication in liver fibrosis. Here we show that hepatic PTP1B mRNA expression increased after bile duct ligation (BDL), while BDL-induced liver fibrosis was markedly reduced in mice lacking Ptpn1 (PTP1B−/−) as assessed by decreased collagen deposition and α-smooth muscle actin (α-SMA) expression. PTP1B−/− mice also showed a significant increase in mRNA levels of key markers of monocytes recruitment (Cd68, Adgre1 and Ccl2) compared to their wild-type (PTP1B+…

0301 basic medicineLiver CirrhosisMaleClinical BiochemistryGene ExpressionApoptosisBiochemistryMice0302 clinical medicineFibrosisTransforming Growth Factor betaRNA Small Interferinglcsh:QH301-705.5Liver injuryProtein Tyrosine Phosphatase Non-Receptor Type 1lcsh:R5-920NADPH oxidaseProtein tyrosine phosphatase 1BbiologyChemistryNOX4Bile duct ligationImmunohistochemistry3. Good healthNOX1Femalelcsh:Medicine (General)hormones hormone substitutes and hormone antagonistsResearch PaperBone marrow transplantationKupffer CellsLiver fibrosisdigestive systemCell LineBile Acids and Salts03 medical and health sciencesmedicineHepatic Stellate CellsAnimalsInflammationOrganic Chemistrymedicine.diseaseMolecular biologyTransplantationDisease Models Animal030104 developmental biologylcsh:Biology (General)Culture Media ConditionedNADPH oxidasesHepatic stellate cellbiology.proteinHepatocytesHepatic fibrosisReactive Oxygen Species030217 neurology & neurosurgeryBiomarkersRedox Biology
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Amphiregulin contained in NSCLC-exosomes induces osteoclast differentiation through the activation of EGFR pathway

2017

AbstractNon-small cell lung cancer (NSCLC) remains the leading cause of cancer-related deaths worldwide. The majority of patients are diagnosed in advanced disease stage. Bone metastasis is the most frequent complication in NSCLC resulting in osteolytic lesions. The perfect balance between bone-resorbing osteoclasts and bone-forming osteoblasts activity is lost in bone metastasis, inducing osteoclastogenesis. In NSCLC, the epidermal growth factor receptor (EGFR) pathway is constitutively activated. EGFR binds Amphiregulin (AREG) that is overexpressed in several cancers such as colon, breast and lung. Its levels in plasma of NSCLC patients correlate with poor prognosis and AREG was recently …

0301 basic medicineLung NeoplasmsCellular differentiationAmphiregulin exosomes NSCLC EGFROsteoclastsExosomes NSCLC AmphiregulinNSCLCExosomesMice0302 clinical medicineSettore BIO/13 - Biologia ApplicataCarcinoma Non-Small-Cell LungMedicineEpidermal growth factor receptorRNA Small InterferingMultidisciplinarybiologyQProteolytic enzymesRBone metastasisCell Differentiation3. Good healthErbB ReceptorsGene Expression Regulation Neoplasticmedicine.anatomical_structureRANKL030220 oncology & carcinogenesisMedicineEngineering sciences. TechnologySciencePrimary Cell CultureBone NeoplasmsAmphiregulinArticle03 medical and health sciencesAmphiregulinOsteoclastCell Line TumorAnimalsHumansbusiness.industryRANK LigandBiological Transportmedicine.diseaseMicrovesiclesCoculture Techniquesrespiratory tract diseases030104 developmental biologyRAW 264.7 CellsImmunologybiology.proteinCancer researchbusiness
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MET-EGFR dimerization in lung adenocarcinoma is dependent on EGFR mtations and altered by MET kinase inhibition

2017

Advanced lung cancer has poor survival with few therapies. EGFR tyrosine kinase inhibitors (TKIs) have high response rates in patients with activating EGFR mutations, but acquired resistance is inevitable. Acquisition of the EGFR T790M mutation causes over 50% of resistance; MET amplification is also common. Preclinical data suggest synergy between MET and EGFR inhibitors. We hypothesized that EGFR-MET dimerization determines response to MET inhibition, depending on EGFR mutation status, independently of MET copy number. We tested this hypothesis by generating isogenic cell lines from NCI-H1975 cells, which co-express L858R and T790M EGFR mutations, namely H1975L858R/T790M (EGFR TKI resista…

0301 basic medicineLung NeoplasmsKinase InhibitorsCancer Treatmentlcsh:MedicinePhysical ChemistryBiochemistryFluorophotometryT790MSpectrum Analysis Techniques0302 clinical medicineFluorescence Resonance Energy TransferMedicine and Health SciencesPhosphorylationEnzyme Inhibitorslcsh:ScienceExtracellular Signal-Regulated MAP KinasesEGFR inhibitorsStainingMice Inbred BALB CMultidisciplinaryFluorescent in Situ HybridizationPhysicsCell StainingProto-Oncogene Proteins c-metPrecipitation TechniquesErbB ReceptorsChemistryOncologySpectrophotometry030220 oncology & carcinogenesisPhysical SciencesErlotinibDimerizationProtein BindingResearch Articlemedicine.drugChemical physicsMice NudeMolecular Probe TechniquesAdenocarcinoma of LungAdenocarcinomaBiologyResearch and Analysis Methods03 medical and health sciencesGefitinibGrowth factor receptorCell Line TumormedicineAnimalsHumansImmunoprecipitationMolecular Biology TechniquesLung cancerProtein Kinase InhibitorsMolecular BiologyCell ProliferationCell growthlcsh:RReproducibility of ResultsBiology and Life SciencesDimers (Chemical physics)medicine.diseaseMolecular biologyIsogenic human disease modelsProbe Hybridizationrespiratory tract diseasesHEK293 Cells030104 developmental biologyChemical PropertiesSpecimen Preparation and TreatmentFocal Adhesion Protein-Tyrosine KinasesMutationEnzymologylcsh:QProtein MultimerizationProto-Oncogene Proteins c-aktCytogenetic TechniquesPLOS ONE
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VEGF-R2/Caveolin-1 Pathway of Undifferentiated ARPE-19 Retina Cells: A Potential Target as Anti-VEGF-A Therapy in Wet AMD by Resvega, an Omega-3/Poly…

2021

Age-related macular degeneration (AMD) is one of the main causes of deterioration in vision in adults aged 55 and older. In spite of therapies, the progression of the disease is often observed without reverse vision quality. In the present study, we explored whether, in undifferentiated ARPE-19 retinal cells, a disruption of the VEGF receptors (VEGF-R)/caveolin-1 (Cav-1)/protein kinases pathway could be a target for counteracting VEGF secretion. We highlight that Resvega®, a combination of omega-3 fatty acids with an antioxidant, resveratrol, inhibits VEGF-A secretion in vitro by disrupting the dissociation of the VEGF-R2/Cav-1 complex into rafts and subsequently preventing MAPK activation.…

0301 basic medicineMAP Kinase Signaling SystemAngiogenesisQH301-705.5Caveolin 1Drug Evaluation PreclinicalresveratrolResveratrolAMDRetinaArticleCatalysisCell LineVEGF-receptorInorganic ChemistryMacular Degeneration03 medical and health scienceschemistry.chemical_compoundangiogenesis0302 clinical medicinemedicineHumansSecretionPhysical and Theoretical ChemistryBiology (General)Molecular BiologyQD1-999SpectroscopyRetinaomega-3 fatty acidsKinaseOrganic Chemistryocular diseasesRetinalGeneral MedicineVascular Endothelial Growth Factor Receptor-2VEGFIn vitroComputer Science ApplicationsTranscription Factor AP-1Chemistry030104 developmental biologymedicine.anatomical_structurechemistry030220 oncology & carcinogenesisCaveolin 1Cancer researchInternational Journal of Molecular Sciences
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CXCR7 Reactivates ERK Signaling to Promote Resistance to EGFR Kinase Inhibitors in NSCLC

2019

Abstract Although EGFR mutant–selective tyrosine kinase inhibitors (TKI) are clinically effective, acquired resistance can occur by reactivating ERK. We show using in vitro models of acquired EGFR TKI resistance with a mesenchymal phenotype that CXCR7, an atypical G protein-coupled receptor, activates the MAPK–ERK pathway via β-arrestin. Depletion of CXCR7 inhibited the MAPK pathway, significantly attenuated EGFR TKI resistance, and resulted in mesenchymal-to-epithelial transition. CXCR7 overexpression was essential in reactivation of ERK1/2 for the generation of EGFR TKI–resistant persister cells. Many patients with non–small cell lung cancer (NSCLC) harboring an EGFR kinase domain mutatio…

0301 basic medicineMAPK/ERK pathwayCancer ResearchLung NeoplasmsDrug ResistanceDrug resistanceTransgenicMiceChemokine receptor0302 clinical medicineNeoplasmsCarcinoma Non-Small-Cell LungReceptorsMedicineNon-Small-Cell LungCXCRReceptorLungbeta-ArrestinsCancerEGFR inhibitorsTumorKinaseLung CancerErbB ReceptorsOncology5.1 Pharmaceuticals030220 oncology & carcinogenesisDevelopment of treatments and therapeutic interventionsTyrosine kinaseEpithelial-Mesenchymal TransitionMAP Kinase Signaling SystemOncology and CarcinogenesisMice TransgenicArticleCell LineExperimental03 medical and health sciencesClinical ResearchCell Line TumorAnimalsHumansOncology & CarcinogenesisProtein Kinase InhibitorsReceptors CXCRbusiness.industryCarcinomaNeoplasms Experimentalrespiratory tract diseases030104 developmental biologyProtein kinase domainDrug Resistance NeoplasmMutationCancer researchNeoplasmbusinessCancer Research
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Noncanonical GLI1 signaling promotes stemness features and in vivo growth in lung adenocarcinoma

2016

Aberrant Hedgehog/GLI signaling has been implicated in a diverse spectrum of human cancers, but its role in lung adenocarcinoma (LAC) is still under debate. We show that the downstream effector of the Hedgehog pathway, GLI1, is expressed in 76% of LACs, but in roughly half of these tumors, the canonical pathway activator, Smoothened, is expressed at low levels, possibly owing to epigenetic silencing. In LAC cells including the cancer stem cell compartment, we show that GLI1 is activated noncanonically by MAPK/ERK signaling. Different mechanisms can trigger the MAPK/ERK/GLI1 cascade including KRAS mutation and stimulation of NRP2 by VEGF produced by the cancer cells themselves in an autocrin…

0301 basic medicineMAPK/ERK pathwayCancer ResearchLung NeoplasmsPyridinesPyridineMitogen-Activated Protein Kinase KinaseMice SCIDMiceCarcinoma Non-Small-Cell LungRNA Small InterferingNon-Small-Cell LungMolecular Biology; Genetics; Cancer ResearchTumorbiologyintegumentary systemHedgehog signaling pathwayCell biologyNeoplastic Stem CellsFemaleRNA InterferenceOriginal ArticleHumanXenograft Model Antitumor AssayAdenocarcinomaSCIDSmall InterferingZinc Finger Protein GLI1Cell LineProto-Oncogene Proteins p21(ras)Adenocarcinoma; Animals; Carcinoma Non-Small-Cell Lung; Cell Line Tumor; Female; Humans; Lung Neoplasms; Mice; Mice SCID; Mitogen-Activated Protein Kinase Kinases; Neoplastic Stem Cells; Neuropilin-2; Proto-Oncogene Proteins p21(ras); Pyridines; Pyrimidines; RNA Interference; RNA Small Interfering; Xenograft Model Antitumor Assays; Zinc Finger Protein GLI1; Molecular Biology; Genetics; Cancer Research03 medical and health sciencesParacrine signallingGeneticSettore MED/04 - PATOLOGIA GENERALEstem cellsCancer stem cellGLI1Cell Line TumorGeneticsAnimalsHumansAutocrine signallingMolecular BiologyMitogen-Activated Protein Kinase KinasesSettore MED/06 - ONCOLOGIA MEDICAAnimalCarcinomaXenograft Model Antitumor AssaysNeuropilin-2Lung Neoplasmlung cancer030104 developmental biologyPyrimidinesPyrimidineCancer cellbiology.proteinRNANeoplastic Stem CellSmoothened
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Uncovering the Signaling Pathway behind Extracellular Guanine-Induced Activation of NO System: New Perspectives in Memory-Related Disorders

2018

Mounting evidence suggests that the guanine-based purines stand out as key player in cell metabolism and in several models of neurodegenerative disorders, such as Parkinson's and Alzheimer's diseases. Guanosine (GUO) and guanine (GUA) are extracellular signaling molecules derived from the breakdown of the correspondent nucleotide, GTP, and their intracellular and extracellular levels are regulated by the fine-tuned activity of two major enzymes, purine nucleoside phosphorylase (PNP) and guanine deaminase (GDA). Noteworthy, GUO and GUA, seem to play opposite roles in the modulation of cognitive functions, such as learning and memory. Indeed GUO, despite exerting neuroprotective, anti-apoptot…

0301 basic medicineMAPK/ERK pathwayCell signalingGuanineGuanosine03 medical and health scienceschemistry.chemical_compoundGuanine deaminase0302 clinical medicineCGMP; ERK; Guanine; L-NAME; Nitric oxide; SH-SY5Y cell line; Pharmacology; Pharmacology (medical)L-NAMEnitric oxideExtracellularguaninePharmacology (medical)Original ResearchPharmacologyChemistrylcsh:RM1-950Cell biologycGMPERKlcsh:Therapeutics. Pharmacology030104 developmental biologySignal transductionSH-SY5Y cell line030217 neurology & neurosurgeryIntracellularFrontiers in Pharmacology
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Therapeutic resistance in breast cancer cells can result from deregulated EGFR signaling

2020

The epidermal growth factor receptor (EGFR) interacts with various downstream molecules including phospholipase C (PLC)/protein kinase C (PKC), Ras/Raf/MEK/ERK, PI3K/PTEN/Akt/GSK-3, Jak/STAT and others. Often these pathways are deregulated in human malignancies such as breast cancer. Various therapeutic approaches to inhibit the activity of EGFR family members including small molecule inhibitors and monoclonal antibodies (MoAb) have been developed. A common problem with cancer treatments is the development of drug-resistance. We examined the effects of a conditionally-activated EGFR (v-Erb-B:ER) on the resistance of breast cancer cells to commonly used chemotherapeutic drugs such as doxorub…

0301 basic medicineMAPK/ERK pathwayEGFRvIIICancer ResearchEGFREstrogen receptorAntineoplastic AgentsBreast Neoplasms03 medical and health sciences0302 clinical medicineBreast cancerBreast cancerCell Line TumorGeneticsHumansMedicinePTENEpidermal growth factor receptorskin and connective tissue diseasesMolecular BiologyProtein kinase BPI3K/AKT/mTOR pathwaybiologybusiness.industryCancermedicine.diseaseErbB Receptors030104 developmental biologyDrug Resistance Neoplasm030220 oncology & carcinogenesisDrug resistancebiology.proteinCancer researchMolecular MedicineFemalebusinessSignal TransductionV-Erb-B
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