Search results for "FIBROBLASTS"

showing 10 items of 445 documents

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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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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Innate Sensing through Mesenchymal TLR4/MyD88 Signals Promotes Spontaneous Intestinal Tumorigenesis

2019

Summary MyD88, an adaptor molecule downstream of innate pathways, plays a significant tumor-promoting role in sporadic intestinal carcinogenesis of the Apcmin/+ model, which carries a mutation in the Apc gene. Here, we show that deletion of MyD88 in intestinal mesenchymal cells (IMCs) significantly reduces tumorigenesis in this model. This phenotype is associated with decreased epithelial cell proliferation, altered inflammatory and tumorigenic immune cell infiltration, and modified gene expression similar to complete MyD88 knockout mice. Genetic deletion of TLR4, but not interleukin-1 receptor (IL-1R), in IMCs led to altered molecular profiles and reduction of intestinal tumors similar to …

0301 basic medicineCarcinogenesisBiologymedicine.disease_causeArticleGeneral Biochemistry Genetics and Molecular BiologyExtracellular matrixMice03 medical and health sciences0302 clinical medicinemedicinetumor microenvironmentAnimalsHumansReceptorinnate immunityTumor microenvironmentInnate immune systemMesenchymal stem cellCell biologyIntestinesToll-Like Receptor 4030104 developmental biologyMyeloid Differentiation Factor 88Knockout mouseTLR4Carcinogenesiscancer-associated fibroblasts030217 neurology & neurosurgerySignal Transduction
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Inflammatory Response Mechanisms of the Dentine–Pulp Complex and the Periapical Tissues

2021

The macroscopic and microscopic anatomy of the oral cavity is complex and unique in the human body. Soft-tissue structures are in close interaction with mineralized bone, but also dentine, cementum and enamel of our teeth. These are exposed to intense mechanical and chemical stress as well as to dense microbiologic colonization. Teeth are susceptible to damage, most commonly to caries, where microorganisms from the oral cavity degrade the mineralized tissues of enamel and dentine and invade the soft connective tissue at the core, the dental pulp. However, the pulp is well-equipped to sense and fend off bacteria and their products and mounts various and intricate defense mechanisms. The fron…

0301 basic medicineCarcinogenesisRoot canalReviewimmune responselcsh:Chemistryodontoblast0302 clinical medicinePulpitislcsh:QH301-705.5SpectroscopyTissue homeostasisOdontoblastsPeriapical TissueIntracellular Signaling Peptides and ProteinsGeneral MedicineComputer Science ApplicationsCell biologyPeriradicularmedicine.anatomical_structureCarcinoma Squamous CellMouth NeoplasmsChemokinescarious lesionPeriapical GranulomaConnective tissueDental CariesBiologyNitric OxideCatalysisInorganic Chemistry03 medical and health sciencestertiary dentinestomatognathic systemAntigens NeoplasmmedicineAnimalsHumansddc:610Physical and Theoretical ChemistryApical foramenMolecular BiologyDental PulpRadicular CystNeuropeptidesOrganic ChemistryPulpitisMesenchymal Stem CellsComplement System Proteins030206 dentistryFibroblastsmedicine.diseasestomatognathic diseases030104 developmental biologyOdontoblastlcsh:Biology (General)lcsh:QD1-999DentinPulp (tooth)Nerve NetPeriapical PeriodontitisInternational Journal of Molecular Sciences
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Alkaline phosphatase dual-binding sites for collagen dictate cell migration and microvessel assembly in vitro

2020

Interactions between cell types, growth factors, and extracellular matrix components involved in angiogenesis are crucial for new vessel formation leading to tissue regeneration. This study investigated whether cocultures of fibroblasts and endothelial cells (ECs; from macro- or microvasculature) play a role in the formation of microvessel-like structures by ECs, as well as modulate fibroblast differentiation and growth factors production (vascular endothelial cell growth factor, basic fibroblast growth factor, active transforming growth factor-beta 1, and interleukin-8), which are important for vessel sprouting and maturation. Data obtained revealed that in vitro coculture systems of fibro…

0301 basic medicineCell typeAngiogenesisProtein ConformationBasic fibroblast growth factorNeovascularization PhysiologicIn Vitro TechniquesBiochemistryExtracellular matrix03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCell MovementmedicineHumansFibroblastMolecular BiologyMicrovesselCells CulturedCell ProliferationBinding SitesChemistryHealth sciences Medical and Health sciencesCiências médicas e da saúdeCell migrationCell DifferentiationCell BiologyFibroblastsAlkaline PhosphataseCell biology030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisMicrovesselsMedical and Health sciencesAlkaline phosphataseCollagenEndothelium VascularCiências da Saúde Ciências médicas e da saúde
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Loss-of-Function Mutations in UNC45A Cause a Syndrome Associating Cholestasis, Diarrhea, Impaired Hearing, and Bone Fragility

2018

International audience; Despite the rapid discovery of genes for rare genetic disorders, we continue to encounter individuals presenting with syndromic manifestations. Here, we have studied four affected people in three families presenting with cholestasis, congenital diarrhea, impaired hearing, and bone fragility. Whole-exome sequencing of all affected individuals and their parents identified biallelic mutations in Unc-45 Myosin Chaperone A (UNC45A) as a likely driver for this disorder. Subsequent in vitro and in vivo functional studies of the candidate gene indicated a loss-of-function paradigm, wherein mutations attenuated or abolished protein activity with concomitant defects in gut dev…

0301 basic medicineDiarrheaMaleCandidate geneAdolescentBone fragilityArticleBone and Bones03 medical and health sciencesYoung AdultCholestasisLoss of Function MutationGCUNC-45MyosinGeneticsMedicineAnimalsHumansFamilyLymphocytes[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsHearing LossGeneGenetics (clinical)Loss functionZebrafishCholestasisbusiness.industryInfant NewbornIntracellular Signaling Peptides and ProteinsSyndromeFibroblastsmedicine.disease3. Good healthPedigreeDiarrhea030104 developmental biologyPhenotype[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsConcomitantChild PreschoolImmunologyFemalemedicine.symptombusinessGastrointestinal Motility
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In vitro cytotoxic effects of DEHP-alternative plasticizers and their primary metabolites on a L929 cell line

2017

IF 4.208; International audience; Phthalic acid esters have been widely used to improve the plasticity of PVC medical devices. They carry a high exposure risk for both humans and the environment in clinical situations. Our study focuses on the cytotoxicity of alternative plasticizers. Postulated primary metabolites were synthesized, not being commercially available. Cytotoxicity assays were performed on L929 murine cells according to the ISO-EN 10993-5 standard design for the biocompatibility of medical devices. The tested concentrations of plasticizers (0.01, 0.05 and 0.1 mg/ml) covered the range likely to be found in biological fluids coming into direct contact with the medical devices. D…

0301 basic medicineEnvironmental EngineeringMetabolite synthesisBiocompatibilityCell SurvivalCytotoxicityHealth Toxicology and MutagenesisMetabolitePhthalic AcidsIn Vitro TechniquesDEHP-alternative plasticizers010501 environmental sciences01 natural sciences[ SDE ] Environmental SciencesMice03 medical and health scienceschemistry.chemical_compoundPhthalatesPlasticizersIn vivoDiethylhexyl PhthalateAnimalsEnvironmental ChemistryOrganic chemistryPolyvinyl ChlorideCytotoxicityCells Cultured0105 earth and related environmental sciences[SDV.MHEP.RSOA] Life Sciences [q-bio]/Human health and pathology/Rhumatology and musculoskeletal systemChromatography[SDV.MHEP.GEG] Life Sciences [q-bio]/Human health and pathology/Geriatry and gerontology[SDV.MHEP.GEG]Life Sciences [q-bio]/Human health and pathology/Geriatry and gerontologyPublic Health Environmental and Occupational HealthPlasticizerPrimary metaboliteEstersGeneral MedicineGeneral ChemistryFibroblastsPollutionIn vitro3. Good healthPhthalic acid030104 developmental biology[SDV.MHEP.RSOA]Life Sciences [q-bio]/Human health and pathology/Rhumatology and musculoskeletal systemchemistryChemosphere
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