Search results for "regulation"

showing 10 items of 4463 documents

Targeting Angiogenesis in Biliary Tract Cancers: An Open Option

2017

Abstract: Biliary tract cancers (BTCs) are characterized by a bad prognosis and the armamentarium of drugs for their treatment is very poor. Although the inflammatory status of biliary tract represents the first step in the cancerogenesis, the microenvironment also plays a key role in the pathogenesis of BTCs, promoting tumor angiogenesis, invasion and metastasis. Several molecules, such as vascular endothelial growth factor (VEGF) and fibroblast growth factor (FGF), are involved in the angiogenesis process and their expression on tumor samples has been explored as prognostic marker in both cholangiocarcinoma and gallbladder cancer. Recent studies evaluated the genomic landscape of BTCs and…

0301 basic medicineMAPK/ERK pathwayVascular Endothelial Growth Factor AAngiogenesisDrug Evaluation PreclinicalTyrosine kinase inhibitorAngiogenesis InhibitorsReviewFibroblast growth factorCatalysiMetastasisAntineoplastic Agentlcsh:Chemistrychemistry.chemical_compoundangiogenesis0302 clinical medicinetyrosine kinase inhibitorsMolecular Targeted Therapylcsh:QH301-705.5SpectroscopyClinical Trials as TopicMonoclonal antibodieNeovascularization Pathologicvascular endothelial growth factorComputer Science Applications1707 Computer Vision and Pattern RecognitionGeneral MedicineComputer Science ApplicationsVascular endothelial growth factorGene Expression Regulation NeoplasticAngiogenesiChemistryBiliary Tract NeoplasmsTreatment OutcomeBiliary Tract Neoplasm030220 oncology & carcinogenesismonoclonal antibodiesTyrosine kinaseAngiogenesis InhibitorHumanSignal TransductionProtein Kinase InhibitorAntineoplastic Agentsbiliary tract cancersBiologyModels BiologicalAngiogenesis; Biliary tract cancers; Monoclonal antibodies; Tyrosine kinase inhibitors; Vascular endothelial growth factor; Angiogenesis Inhibitors; Animals; Antineoplastic Agents; Biliary Tract Neoplasms; Clinical Trials as Topic; Drug Evaluation Preclinical; Gene Expression Regulation Neoplastic; Genetic Variation; Humans; Models Biological; Neovascularization Pathologic; Protein Kinase Inhibitors; Signal Transduction; Treatment Outcome; Vascular Endothelial Growth Factor A; Molecular Targeted Therapy; Catalysis; Molecular Biology; Spectroscopy; Computer Science Applications1707 Computer Vision and Pattern Recognition; Physical and Theoretical Chemistry; Organic Chemistry; Inorganic ChemistryCatalysisInorganic Chemistry03 medical and health sciencesIn vivomedicineAnimalsHumansPhysical and Theoretical ChemistryGallbladder cancerMolecular BiologyProtein Kinase InhibitorsBiologyAnimalOrganic ChemistryGenetic Variationmedicine.disease030104 developmental biologychemistrylcsh:Biology (General)lcsh:QD1-999Immunologyangiogenesis; biliary tract cancers; monoclonal antibodies; tyrosine kinase inhibitors; vascular endothelial growth factorCancer researchBiliary tract cancerInternational Journal of Molecular Sciences
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NEGR1 and FGFR2 cooperatively regulate cortical development and core behaviours related to autism disorders in mice.

2018

See Contreras and Hippenmeyer (doi:10.1093/brain/awy218) for a scientific commentary on this article. Autism spectrum disorders (ASDs) are complex conditions with diverse aetiologies. Szczurkowska et al. demonstrate that two ASD-related molecules – FGFR2 and Negr1 – physically interact to act on the same downstream pathway, and regulate cortical development and ASD-relevant behaviours in mice. Identifying common mechanisms in ASDs may reveal targets for pharmacological intervention.

0301 basic medicineMAPK/ERK pathwaygenetic structuresAutism Spectrum DisorderFGFR2 signalingFibroblast growth factorReceptor tyrosine kinaseMiceautism; development; cell adhesion; in utero electroporation; FGFR2 signaling0302 clinical medicineCell MovementCerebral CortexMice KnockoutbiologyBehavior AnimalKinaseCell adhesion moleculeCell biologyProtein TransportSignal Transductionmusculoskeletal diseasesMAP Kinase Signaling SystemCell Adhesion Molecules NeuronalDendritic SpinesNeurogenesisautismDown-Regulationbehavioral disciplines and activities03 medical and health sciencesmental disordersmedicineAnimalsHumansAutistic DisorderReceptor Fibroblast Growth Factor Type 2developmentProtein kinase BFibroblast growth factor receptor 2Cell Membranecell adhesionOriginal Articlesin utero electroporationmedicine.diseaseMice Inbred C57BLDisease Models Animal030104 developmental biologyHEK293 Cellsbiology.proteinAutismNeurology (clinical)030217 neurology & neurosurgeryBrain : a journal of neurology
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Potential Therapeutic Applications of MDA-9/Syntenin-NF-κB-RKIP Loop in Human Liver Carcinoma

2019

Background Overexpression of MDA-9/Syntenin occurs in multiple human cancer cell lines and is associated with higher grade of tumor classification, invasiveness and metastasis. In some cases, its role in cancer biology depends on relationships between MDA-9/Syntenin and NF-κB. Objective This study aims to analyze the presence of a regulation loop like that between MDA-9/Syntenin - NF-κB - RKIP in human liver carcinoma. Methods Transient transfection was performed with siRNA anti-MDA-9/Syntenin. Expression of different factors was evaluated by Real time-PCR and Western blotting, while NF-κB activation by TransAM assay. Invasion capacity was analyzed by Matrigel Invasion Assay and the effects…

0301 basic medicineMDA-9/Syntenin NF-κB RKIP drug targets HA22T/VGH Hep3B HepG2Carcinoma HepatocellularCurcuminSynteninsPhosphatidylethanolamine Binding ProteinBiochemistry03 medical and health scienceschemistry.chemical_compound0302 clinical medicineDownregulation and upregulationAntineoplastic Combined Chemotherapy ProtocolsHumansGene silencingNeoplasm InvasivenessViability assayMolecular BiologyCell growthMatrigel Invasion AssayLiver NeoplasmsNF-kappa BNF-κBHep G2 CellsGeneral MedicineNeoplasm ProteinsBlot030104 developmental biologychemistryDoxorubicinCell cultureSettore BIO/14 - FarmacologiaCancer researchMolecular MedicineSignal Transduction030215 immunologyCurrent Molecular Medicine
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Unusual roles of caspase-8 in triple-negative breast cancer cell line MDA-MB-231

2015

Triple-negative breast cancer (TNBC) is a clinically aggressive form of breast cancer that is unresponsive to endocrine agents or trastuzumab. TNBC accounts for ~10-20% of all breast cancer cases and represents the form with the poorest prognosis. Patients with TNBC are at higher risk of early recurrence, mainly in the lungs, brain and soft tissue, therefore, there is an urgent need for new therapies. The present study was carried out in MDA-MB-231 cells, where we assessed the role of caspase-8 (casp-8), a critical effector of death receptors, also involved in non‑apoptotic functions. Analysis of casp-8 mRNA and protein levels indicated that they were up-regulated with respect to the normal…

0301 basic medicineMDA-MB-231 cellCancer ResearchDown-RegulationTriple Negative Breast NeoplasmsTransfectionResting Phase Cell Cycle03 medical and health sciencesKruppel-Like Factor 40302 clinical medicineHMGA2Breast cancerCell Line TumormedicineHumansRNA Small InterferingCaspase-8 unusual roleTriple-negative breast cancerCaspase 8Triple-negative breast cancer cellbiologyOncogeneCaspase-8 knockdownCell CycleG1 PhaseCancerCell cyclemedicine.diseaseMolecular medicineKLF4Invasivity and metastasi030104 developmental biologyOncologyKLF4030220 oncology & carcinogenesisbiology.proteinCancer researchFemaleCell cycle regulator
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Effects of Ranolazine on Astrocytes and Neurons in Primary Culture.

2016

Ranolazine (Rn) is an antianginal agent used for the treatment of chronic angina pectoris when angina is not adequately controlled by other drugs. Rn also acts in the central nervous system and it has been proposed for the treatment of pain and epileptic disorders. Under the hypothesis that ranolazine could act as a neuroprotective drug, we studied its effects on astrocytes and neurons in primary culture. We incubated rat astrocytes and neurons in primary cultures for 24 hours with Rn (10-7, 10-6 and 10-5 M). Cell viability and proliferation were measured using trypan blue exclusion assay, MTT conversion assay and LDH release assay. Apoptosis was determined by Caspase 3 activity assay. The …

0301 basic medicineMacroglial CellsPhysiologyInterleukin-1betaProtein ExpressionCell Culture Techniqueslcsh:MedicineApoptosisPharmacologyPathology and Laboratory Medicine0302 clinical medicineRanolazineAnimal CellsImmune PhysiologyMedicine and Health SciencesEnzyme assaysColorimetric assaysEnzyme-Linked Immunoassayslcsh:ScienceBioassays and physiological analysisImmune ResponseNeuronsInnate Immune SystemMultidisciplinaryMTT assayCell DeathCaspase 3medicine.anatomical_structureCell ProcessesCytokinesTumor necrosis factor alphaCellular TypesAstrocyteResearch ArticleProgrammed cell deathCell SurvivalImmunologyCaspase 3Glial CellsBiologyGene Expression Regulation EnzymologicMitochondrial Proteins03 medical and health sciencesSigns and SymptomsmedicineGene Expression and Vector TechniquesAnimalsMTT assayViability assayMolecular Biology TechniquesImmunoassaysMolecular BiologyInflammationMolecular Biology Assays and Analysis TechniquesSuperoxide DismutaseTumor Necrosis Factor-alphalcsh:RBiology and Life SciencesCell BiologyMolecular DevelopmentRatsPPAR gammaResearch and analysis methodsOxidative Stress030104 developmental biologyCell cultureApoptosisAstrocytesImmune SystemBiochemical analysisImmunologic Techniqueslcsh:QFisiologia humanaApoptosis Regulatory ProteinsCarrier Proteins030217 neurology & neurosurgeryDevelopmental BiologyPloS one
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miR-128 Is Implicated in Stress Responses by Targeting MAFG in Skeletal Muscle Cells.

2017

MAFG (v-Maf avian musculoaponeurotic fibrosarcoma oncogene homolog G) is a bZIP-type transcriptional regulator that belongs to the small MAF (sMAFs) protein family. By interacting with other bZIP transcription factors, sMAFs can form homo- and heterodimers governing either repressive or activating transcriptional functions. As heterodimeric partner of Nrf2, MAFG positively influences the ARE-dependent antioxidant/xenobiotic pathways, at least in condition of a correct MAFG:Nrf2 balance. MicroRNAs (miRs) participate to different regulatory networks being involved as fine-tuning regulators of gene expression. However, the connections between cellular surveillance to stresses mediated by MAFG:…

0301 basic medicineMafG Transcription FactorMaleAgingProtein familyArticle SubjectNF-E2-Related Factor 2Muscle Fibers SkeletalBiologyTransfectionBiochemistryAntioxidants03 medical and health sciencesMiceGene expressionmicroRNATranscriptional regulationAnimalsHumanslcsh:QH573-671Gene3' Untranslated RegionsGeneticsBinding SitesOncogeneThree prime untranslated regionlcsh:CytologyHEK 293 cellsMembrane ProteinsCell BiologyGeneral MedicineMice Inbred C57BLRepressor ProteinsMicroRNAsOxidative Stress030104 developmental biologyHEK293 CellsHeme Oxygenase-1Research ArticleOxidative medicine and cellular longevity
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DNA methylomes reveal biological networks involved in human eye development, functions and associated disorders

2017

This work provides a comprehensive CpG methylation landscape of the different layers of the human eye that unveils the gene networks associated with their biological functions and how these are disrupted in common visual disorders. Herein, we firstly determined the role of CpG methylation in the regulation of ocular tissue-specification and described hypermethylation of retinal transcription factors (i.e., PAX6, RAX, SIX6) in a tissue-dependent manner. Second, we have characterized the DNA methylome of visual disorders linked to internal and external environmental factors. Main conclusions allow certifying that crucial pathways related to Wnt-MAPK signaling pathways or neuroinflammation are…

0301 basic medicineMaleADNlcsh:MedicineUllRetinal NeovascularizationEyeEpigenesis Genetic0302 clinical medicinelcsh:ScienceChildCàncerCancerRegulation of gene expressionMultidisciplinaryRetinoblastomaMelanomaMethylationDNA NeoplasmOphthalmopathiesNeoplasm ProteinsGene Expression Regulation NeoplasticOftalmologiaChild PreschoolDNA methylationFemaleMetilacióOftalmopatiesAdultMAP Kinase Signaling SystemBiologyMethylationArticle03 medical and health sciencesETS1medicineHumansEye ProteinsTranscription factorDiabetic RetinopathyEye Neoplasmslcsh:RDNADNA Methylationmedicine.diseaseeye diseasesOphthalmology030104 developmental biologyImmunology030221 ophthalmology & optometryCancer researchlcsh:QPAX6
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Peroxisome proliferator-activated receptor alpha deficiency impairs regulatory T cell functions: Possible application in the inhibition of melanoma t…

2016

International audience; Regulatory T (Treg) cells are important to induce and maintain immunological self-tolerance. Although the progress accomplished in understanding the functional mechanism of Treg cells, intracellular molecules that control the mechanisms of their suppressive capacity are still on investigation. The present study showed that peroxisome proliferator-activated receptor-alpha deficiency impaired the suppressive activity of Treg cells on CD4(+)CD25(-) and CD8(+) T cell proliferation. In Treg cells, PPARα gene deletion also induced a decrease of migratory abilities, and downregulated the expression of chemokine receptors (CCR-4, CCR-8 and CXCR-4) and p27(KIP1) mRNA. Treg ce…

0301 basic medicineMaleAdoptive cell transferMESH: Tumor BurdenB16 melanoma tumorMelanoma ExperimentalMESH: T-Lymphocyte SubsetsCD4(+)CD25(+) regulatory T cellsBiochemistryMESH: Mice KnockoutImmunotherapy AdoptiveT-Lymphocytes RegulatoryPPARαMESH : T-Lymphocytes RegulatoryCell MovementT-Lymphocyte SubsetsMESH: Reverse Transcriptase Polymerase Chain ReactionMESH : Cell ProliferationMESH : Cell MovementMESH: AnimalsIL-2 receptorMESH: PPAR alphaMESH: Cell MovementCells CulturedMice KnockoutMESH : Melanoma ExperimentalbiologyMESH : Tumor BurdenReverse Transcriptase Polymerase Chain ReactionMESH : Reverse Transcriptase Polymerase Chain ReactionFOXP3hemic and immune systemsGeneral MedicineMESH: Gene Expression Regulation Neoplastic3. Good healthTumor BurdenMESH: Melanoma ExperimentalDNA-Binding ProteinsGene Expression Regulation Neoplasticmedicine.anatomical_structureMESH: Immunotherapy AdoptiveReceptors ChemokineMESH : DNA-Binding ProteinsMESH: Cells Culturedmedicine.medical_specialtyMESH : Receptors ChemokineMESH: Cell Line TumorRegulatory T cellMESH : Gene Expression Regulation NeoplasticT cellMESH : MaleMESH : PPAR alphachemical and pharmacologic phenomenaMESH : Mice Inbred C57BLMESH : Clonal Anergy03 medical and health sciencesMESH: Mice Inbred C57BLInternal medicineMESH: Cell ProliferationCell Line TumorMESH : Cells CulturedmedicineAnimals[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyPPAR alpha[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyCell ProliferationClonal AnergyPerforinMESH : Cell Line TumorMESH: T-Lymphocytes RegulatoryMolecular biologyMESH: MaleMESH : T-Lymphocyte SubsetsGranzyme BMice Inbred C57BL030104 developmental biologyEndocrinologyPerforinMESH: Clonal Anergybiology.proteinMESH : Mice KnockoutMESH : AnimalsMESH: Receptors ChemokineCD8MESH: DNA-Binding ProteinsMESH : Immunotherapy Adoptive
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Mild exacerbation of obesity- and age-dependent liver disease progression by senolytic cocktail dasatinib + quercetin.

2021

Abstract Background Nonalcoholic fatty liver disease (NAFLD) is increasingly prevalent and represents a growing challenge in terms of prevention and treatment. A minority of affected patients develops inflammation, subsequently fibrosis, cirrhosis and hepatocellular carcinoma (HCC). HCC is a leading cause of cancer-related death. An increased number of senescent cells correlate with age-related tissue degeneration during NAFLD-induced HCC. Senolytics are promising agents that target selectively senescent cells. Previous studies showed that whereas a combination of the senolytic drugs dasatinib and quercetin (D + Q) reduced NAFLD in mice, D + Q lacked efficacy in removing doxorubicin-induced…

0301 basic medicineMaleAgingCirrhosisDasatiniblcsh:MedicineBiochemistrySenolytics.Liver disease0302 clinical medicineFibrosisNon-alcoholic Fatty Liver DiseaseSenotherapeuticsNonalcoholic fatty liver diseaseDiethylnitrosamineCancerlcsh:CytologyLiver Diseases3. Good healthDasatinib030220 oncology & carcinogenesisHepatocellular carcinomaDisease ProgressionQuercetinmedicine.symptomLiver diseasemedicine.drugShort ReportInflammationDiet High-Fat03 medical and health sciencesmedicineAnimalsObesitylcsh:QH573-671SenolyticMolecular BiologyInflammationbusiness.industrySenolyticslcsh:RCell Biologymedicine.diseasedigestive system diseasesMice Inbred C57BLDisease Models Animal030104 developmental biologyGene Expression RegulationCancer researchbusinessCell communication and signaling : CCS
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Aging-associated genes and let-7 microRNAs: a contribution to myogenic program dysregulation in oculopharyngeal muscular dystrophy

2019

Oculopharyngeal muscular dystrophy (OPMD) is a late-onset muscle disease caused by an abnormal (GCN) triplet expansion within the polyadenylate-binding protein nuclear 1 gene and consequent mRNA pr...

0301 basic medicineMaleAgingOculopharyngealMuscle DevelopmentBiochemistryMyoblasts0302 clinical medicine80 and overMuscular DystrophyHMGB1 ProteinPAX7 Transcription FactorCell DifferentiationdifferentiationMiddle AgedCell biologymedicine.anatomical_structureFemaleMyogeninMitogen-Activated Protein KinasesBiotechnologyDifferentiation regeneration skeletal muscleAdultBiologyInclusion BodyOculopharyngeal muscular dystrophy03 medical and health sciencesmicroRNAGeneticsmedicineHumansGenetic Predisposition to Diseasedifferentiation; regeneration; skeletal muscle; Adult; Aged; Aged 80 and over; Aging; Antigens Neoplasm; Cell Differentiation; Female; Gene Expression Regulation; HMGB1 Protein; Humans; Male; MicroRNAs; Middle Aged; Mitogen-Activated Protein Kinases; Muscle Development; Muscular Dystrophy Oculopharyngeal; Myoblasts; Myogenin; Myositis Inclusion Body; PAX7 Transcription Factor; Genetic Predisposition to Diseaseskeletal muscleAntigensMolecular BiologyGeneAgedMessenger RNAMyositisRegeneration (biology)Skeletal musclemedicine.diseaseMicroRNAs030104 developmental biologyMuscle diseaseGene Expression RegulationregenerationNeoplasm030217 neurology & neurosurgery
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