Search results for " Fibroblast"

showing 10 items of 140 documents

Carbamazepine, cadmium chloride and polybrominated diphenyl ether-47, synergistically modulate the expression of antioxidants and cell cycle biomarke…

2019

Abstract A wide range of contaminants, industrial by-products, plastics, and pharmaceutics belonging to various categories, have been found in sea water. Although these compounds are detected at concentrations that might be considered as sub-lethal, under certain conditions they could act synergistically producing unexpected effects in term of toxicity or perturbation of biochemical markers leading to standard pathway. In this study, the Sparus aurata fibroblast cell line SAF-1, was exposed to increasing concentrations of carbamazepine (CBZ), polybrominated diphenyl ether 47 (BDE-47) and cadmium chloride (CdCl2) until 72 h, to evaluate the cytotoxicity and the expression of genes related to…

0106 biological sciencesAntioxidantmedicine.medical_treatmentAquatic ScienceCadmium chlorideOceanographymedicine.disease_cause010603 evolutionary biology01 natural sciencesCell LinePolybrominated diphenyl-etherchemistry.chemical_compoundCadmium ChlorideSettore AGR/20 - ZoocoltureSettore BIO/10 - BiochimicaHalogenated Diphenyl EthersmedicineAnimalsoxidative stressSparus aurata fibroblastSettore BIO/06 - Anatomia Comparata E CitologiaCytotoxicity010604 marine biology & hydrobiologyCell CycleDiphenyl etherbiomarkersBiomarkerGeneral MedicineCell cycleCadmium chloridePollutionEnzyme ActivationOxidative StressCarbamazepineGene Expression RegulationchemistryBiochemistry:5 - Ciencias puras y naturales::57 - Biología::576 - Biología celular y subcelular. Citología [CDU]Cell culturecarbamazepineToxicityOxidative streEnergy MetabolismOxidoreductasespolybrominated diphenyl-etherBiomarkersWater Pollutants ChemicalOxidative stressMarine Environmental Research
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The JAK2 pathway is activated in idiopathic pulmonary fibrosis

2018

Background: Idiopathic pulmonary fibrosis (IPF) is the most rapidly progressive and fatal fibrotic disorder, with no curative therapies. The signal transducer and activator of transcription 3 (STAT3) protein is activated in lung fibroblasts and alveolar type II cells (ATII), thereby contributing to lung fibrosis in IPF. Although activation of Janus kinase 2 (JAK2) has been implicated in proliferative disorders, its role in IPF is unknown. The aim of this study was to analyze JAK2 activation in IPF, and to determine whether JAK2/STAT3 inhibition is a potential therapeutic strategy for this disease. Methods and results: JAK2/p-JAK2 and STAT3/pSTAT3 expression was evaluated using quantitative …

0301 basic medicineAdultMaleSTAT3 Transcription FactorIdiopathic pulmonary fibrosisEpithelial cellsLung fibroblastsFibroblast migrationPulmonary fibrosisSTAT303 medical and health sciencesIdiopathic pulmonary fibrosisFibrosishemic and lymphatic diseasesMedicineAnimalsHumansFibroblastAgedlcsh:RC705-779A549 cellCèl·lules epitelialsLungbiologybusiness.industryResearchFibrosi pulmonarlcsh:Diseases of the respiratory systemTransforming growth factor betaFibroblastsJanus Kinase 2Middle Agedrespiratory systemmedicine.diseaseTriterpenesRatsrespiratory tract diseasesEnzyme Activation030104 developmental biologymedicine.anatomical_structureJAK2A549 CellsAlveolar type II epithelial cellsCancer researchbiology.proteinFemalebusinessMyofibroblastSignal Transduction
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Heat shock protein (Hsp) regulation by muscarinic acetylcholine receptor (mAChR) activation in the rat hippocampus.

2018

The cholinergic system plays a crucial role in modulating in the central nervous system physiological responses such as neurogenesis, neuronal differentiation, synaptic plasticity, and neuroprotection. In a recent study, we showed that Oxotremorine-M, a non-selective muscarinic acetylcholine receptor agonist, is able to transactivate the fibroblast growth factor receptor and to produce a significant increase in the hippocampal primary neurite outgrowth. In the present study we aimed to explore in the rat hippocampus the possible effect of acute or chronic treatment with Oxotremorine-M on some heat shock proteins (Hsp60, Hsp70, Hsp90) and on activation of related transcription factor heat sh…

0301 basic medicineAgonistMalemedicine.medical_specialtymedicine.drug_classPhysiologyClinical BiochemistryNeuronal OutgrowthScopolamineheat shock proteinHsp90NeuroprotectionHippocampusHsp7003 medical and health sciencesmuscarinic receptor0302 clinical medicineHeat Shock Transcription FactorsHeat shock proteinInternal medicineMuscarinic acetylcholine receptormedicineOxotremorineAnimalsRats WistarHSF1Heat-Shock ProteinsNeuronsNeuronal PlasticityChemistryOxotremorineNeurodegenerative DiseasesCell BiologyReceptors Fibroblast Growth FactorReceptors MuscarinicHsp70Rats030104 developmental biologyEndocrinologyheat shock factor 1HSP60030217 neurology & neurosurgerymedicine.drugSignal TransductionJournal of cellular physiology
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Mutant p53 induces Golgi tubulo-vesiculation driving a prometastatic secretome

2020

TP53 missense mutations leading to the expression of mutant p53 oncoproteins are frequent driver events during tumorigenesis. p53 mutants promote tumor growth, metastasis and chemoresistance by affecting fundamental cellular pathways and functions. Here, we demonstrate that p53 mutants modify structure and function of the Golgi apparatus, culminating in the increased release of a pro-malignant secretome by tumor cells and primary fibroblasts from patients with Li-Fraumeni cancer predisposition syndrome. Mechanistically, interacting with the hypoxia responsive factor HIF1α, mutant p53 induces the expression of miR-30d, which in turn causes tubulo-vesiculation of the Golgi apparatus, leading …

0301 basic medicineBiopsyGeneral Physics and AstronomyGolgi ApparatusAnimals Biopsy Breast Neoplasms Cell Line Tumor Cell Transformation Neoplastic Female Fibroblasts Gene Expression Regulation Neoplastic Golgi Apparatus Humans Hypoxia-Inducible Factor 1 alpha Subunit Li-Fraumeni Syndrome Mice MicroRNAs Microtubules Mutation Primary Cell Culture Secretory Vesicles Signal TransductionSkin Tumor Microenvironment Tumor Suppressor Protein p53 Xenograft Model Antitumor Assays02 engineering and technologymedicine.disease_causeCell TransformationMicrotubulesSettore BIO/09 - FisiologiaMetastasisLi-Fraumeni SyndromeMiceTumor MicroenvironmentGolgisecretory machinerySuper-resolution microscopyAnimals; Biopsy; Breast Neoplasms; Cell Line Tumor; Cell Transformation Neoplastic; Female; Fibroblasts; Gene Expression Regulation Neoplastic; Golgi Apparatus; Humans; Hypoxia-Inducible Factor 1 alpha Subunit; Li-Fraumeni Syndrome; Mice; MicroRNAs; Microtubules; Mutation; Primary Cell Culture; Secretory Vesicles; Signal Transduction; Skin; Tumor Microenvironment; Tumor Suppressor Protein p53; Xenograft Model Antitumor Assayslcsh:ScienceSkinMultidisciplinaryTumorChemistrymutant p53QCell migrationMicroRNASecretomics021001 nanoscience & nanotechnologyCell biologyGene Expression Regulation NeoplasticCell Transformation NeoplasticsymbolsFibroblastmiR-30dFemaleHypoxia-Inducible Factor 10210 nano-technologyBreast NeoplasmHumanSignal TransductionCancer microenvironmentStromal cellSecretory VesicleSciencePrimary Cell CultureBreast NeoplasmsMicrotubuleGolgi ApparatuSettore MED/08 - Anatomia Patologicaalpha SubunitGeneral Biochemistry Genetics and Molecular BiologyArticleCell Line03 medical and health sciencessymbols.namesakeCell Line TumormedicineAnimalsHumansSettore MED/05 - Patologia ClinicaSecretionTumor microenvironmentNeoplasticAnimalSecretory VesiclesGeneral ChemistryOncogenesGolgi apparatusHDAC6FibroblastsMicroreviewHypoxia-Inducible Factor 1 alpha SubunitmicroenvironmentXenograft Model Antitumor AssaysMicroRNAs030104 developmental biologyGene Expression RegulationMutationlcsh:QTumor Suppressor Protein p53Carcinogenesis
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Metabolic Cooperation and Competition in the Tumor Microenvironment: Implications for Therapy

2017

The tumor microenvironment (TME) is an ensemble of non-tumor cells comprising fibroblasts, cells of the immune system, and endothelial cells, besides various soluble secretory factors from all cellular components (including tumor cells). The TME forms a pro-tumorigenic cocoon around the tumor cells where reprogramming of the metabolism occurs in tumor and non-tumor cells that underlies the nature of interactions as well as competitions ensuring steady supply of nutrients and anapleoretic molecules for the tumor cells that fuels its growth even under hypoxic conditions. This metabolic reprogramming also plays a significant role in suppressing the immune attack on the tumor cells and in resis…

0301 basic medicineCancer ResearchCell signalingTumor microenvironmentimmune networkReviewBiologymetabolic cooperationcancer cell metabolismWarburg effectCell biology03 medical and health sciences030104 developmental biologyImmune systemOncologyCancer-Associated Fibroblaststumor microenvironmentmetabolic reprogrammingEpigeneticssense organsWarburg effectTranscription factorReprogrammingcancer-associated fibroblastsFrontiers in Oncology
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Isolation, culture and analysis of adult subependymal neural stem cells

2016

Individual cells dissected from the subependymal neurogenic niche of the adult mouse brain proliferate in medium containing basic fibroblast growth factor (bFGF) and/or epidermal growth factor (EGF) as mitogens, to produce multipotent clonal aggregates called neurospheres. These cultures constitute a powerful tool for the study of neural stem cells (NSCs) provided that they allow the analysis of their features and potential capacity in a controlled environment that can be modulated and monitored more accurately than in vivo. Clonogenic and population analyses under mitogen addition or withdrawal allow the quantification of the self-renewing and multilineage potency of these cells and the id…

0301 basic medicineCancer ResearchNeurogenesisCellular differentiationBasic fibroblast growth factorPopulationCell Culture TechniquesBiologyMice03 medical and health scienceschemistry.chemical_compoundNeural Stem CellsEpendymaNeurosphereSubependymal zoneAnimalsHumanseducationMolecular BiologyNeuronseducation.field_of_studyNeurogenesisCell DifferentiationCell BiologyNeural stem cellCell biologyAdult Stem Cells030104 developmental biologychemistryImmunologyDevelopmental BiologyAdult stem cellDifferentiation
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Tumor-Associated Fibroblasts Promote HER2-Targeted Therapy Resistance through FGFR2 Activation

2020

AbstractPurpose:Despite the therapeutic success of existing HER2-targeted therapies, tumors invariably relapse. This study aimed at identifying new mechanisms responsible for HER2-targeted therapy resistance.Experimental Design:We have used a platform of HER2-targeted therapy–resistant cell lines and primary cultures of healthy and tumor-associated fibroblasts (TAF) to identify new potential targets related to tumor escape from anti-HER2 therapies.Results:We have shown that TAFs promote resistance to HER2-targeted therapies. TAFs produce and secrete high levels of FGF5, which induces FGFR2 activation in the surrounding breast cancer cells. FGFR2 transactivates HER2 via c-Src, leading to res…

0301 basic medicineCancer ResearchReceptor ErbB-2medicine.medical_treatmentMice NudeBreast NeoplasmsDrug resistanceTargeted therapy03 medical and health sciencesMice0302 clinical medicineBreast cancerCancer-Associated FibroblastsTrastuzumabCell Line TumorAntineoplastic Combined Chemotherapy ProtocolsmedicineNeoplasmAnimalsHumansReceptor Fibroblast Growth Factor Type 2skin and connective tissue diseasesneoplasmsbusiness.industryLapatinibTrastuzumabmedicine.diseaseXenograft Model Antitumor AssaysSurvival Rate030104 developmental biologyOncologyTumor EscapeApoptosisDrug Resistance Neoplasm030220 oncology & carcinogenesisCancer researchFemaleSignal transductionNeoplasm Recurrence Localbusinessmedicine.drugSignal Transduction
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Cancer-associated fibroblasts as abettors of tumor progression at the crossroads of EMT and therapy resistance

2019

Abstract In the last decades, the role of the microenvironment in tumor progression and therapeutic outcome has gained increasing attention. Cancer-associated fibroblasts (CAFs) have emerged as key players among stromal cells, owing to their abundance in most solid tumors and their diverse tumor-restraining/promoting roles. The interplay between tumor cells and neighboring CAFs takes place by both paracrine signals (cytokines, exosomes and metabolites) or by the multifaceted functions of the surrounding extracellular matrix. Here, we dissect the most recent identified mechanisms underlying CAF-mediated control of tumor progression and therapy resistance, which include induction of the epith…

0301 basic medicineCancer ResearchStromal cellEpithelial-Mesenchymal TransitionParacrine CommunicationAntineoplastic AgentsReviewBiologylcsh:RC254-28203 medical and health sciences0302 clinical medicineCancer-Associated FibroblastsCancer stem cellSettore MED/04 - PATOLOGIA GENERALENeoplasmsParacrine CommunicationTumor MicroenvironmentHumansEpithelial–mesenchymal transitionTumor microenvironmentCancer associated fibroblasts cancer stem cells extracellular matrix exosomes epithelial-to-mesenchymal transition.lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensMicrovesiclesGene Expression Regulation Neoplastic030104 developmental biologyOncologyTumor progressionDrug Resistance Neoplasm030220 oncology & carcinogenesisCancer researchDisease ProgressionMolecular MedicineCancer-Associated FibroblastsSignal Transduction
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Differential distribution and enrichment of non-coding RNAs in exosomes from normal and Cancer-associated fibroblasts in colorectal cancer.

2018

Exosome production from cancer-associated fibroblasts seems to be an important driver of tumor progression. We report the first in-depth biotype characterization of ncRNAs, analyzed by Next Generation Sequencing and Bioinformatics, expressed in established primary human normal and cancer-associated fibroblasts (CAFs) from cancer and normal mucosa tissues from 9 colorectal cancer patients, and/or packaged in their derived exosomes. Differential representation and enrichment analyses based on these ncRNAs revealed a significant number of differences between the ncRNA content of exosomes and the expression patterns of the normal and cancer-associated fibroblast cells. ncRNA regulatory elements…

0301 basic medicineCancer ResearchStromal cellRNA UntranslatedColorectal cancerBiologyExosomeslcsh:RC254-282Non-coding RNAs03 medical and health sciencesCancer-Associated FibroblastsCell MovementNext generation sequencingmedicineBiomarkers TumorHumansLiquid biopsyLetter to the EditorCells CulturedCell ProliferationTumor microenvironmentColon CancerLiquid biopsySequence Analysis RNACancerHigh-Throughput Nucleotide SequencingFibroblastsmedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPrognosisMicrovesiclesGene Expression Regulation Neoplastic030104 developmental biologyOncologyTumor microenvironmentTumor progressionCancer researchMolecular MedicineCancer-Associated FibroblastsColorectal Neoplasms
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Tumor Microenvironment And Epithelial Mesenchymal Transition As Targets To Overcome Tumor Multidrug Resistance

2020

It is well established that multifactorial drug resistance hinders successful cancer treatment. Tumor cell interactions with the tumor microenvironment (TME) are crucial in epithelial-mesenchymal transition (EMT) and multidrug resistance (MDR). TME-induced factors secreted by cancer cells and cancer-associated fibroblasts (CAFs) create an inflammatory microenvironment by recruiting immune cells. CD11b+/Gr-1+ myeloid-derived suppressor cells (MDSCs) and inflammatory tumor associated macrophages (TAMs) are main immune cell types which further enhance chronic inflammation. Chronic inflammation nurtures tumor-initiating/cancer stem-like cells (CSCs), induces both EMT and MDR leading to tumor re…

0301 basic medicineCancer Researchmedicine.medical_treatmentMultidrug resistanceTargeted therapyTargeted therapy0302 clinical medicineCancer-Associated FibroblastsNeoplasmsAntineoplastic Combined Chemotherapy ProtocolsTumor-Associated MacrophagesTumor MicroenvironmentPharmacology (medical)HypoxiaTOR Serine-Threonine KinasesSmall moleculesChemotherapy ; Hypoxia ; Inflammation ; Microenvironment ; Multidrug resistance ; Small molecules ; Targeted therapy.Drug Resistance Multiple3. Good healthDNA DemethylationGene Expression Regulation NeoplasticInfectious DiseasesOncology030220 oncology & carcinogenesisInflammation MediatorsEpithelial-Mesenchymal TransitionStromal cellMicroenvironmentBiologyProinflammatory cytokine03 medical and health sciencesCell Line TumormedicineAnimalsHumansChemotherapyEpithelial–mesenchymal transitionPharmacologyInflammationTumor microenvironmentCancerHypoxia-Inducible Factor 1 alpha Subunitmedicine.diseaseHistone Deacetylase InhibitorsMultiple drug resistanceDisease Models Animal030104 developmental biologyDrug Resistance NeoplasmCancer cellCancer research
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