Search results for "GF"

showing 10 items of 838 documents

Corrigendum: Resolvin D1 Modulates the Intracellular VEGF-Related miRNAs of Retinal Photoreceptors Challenged With High Glucose

2020

Abstract Stimulation of retinal photoreceptors with elevated glucose concentration (30 mM) for 96 hours, served as diabetic retinopathy in-vitro model to study Resolvin D1 (50 nM) effects on neovascularization. VEGF and anti-angiogenic miR-20a-3p, miR-20a-5p, miR-106a-5p and miR-20b expression was assessed either in photoreceptors exposed to HG or in exosomes released by those cells. High glucose increased VEGF levels and concurrently decreased anti-angiogenic miRNAs content in photoreceptors and exosomes. RvD1 reverted the effects of glucose damage in photoreceptors and exosomal pro-angiogenic potential, tested with the HUVEC angiogenesis assay. By activating FPR2 receptor, RvD1 modulated …

0301 basic medicineAngiogenesisStimulationexosomesretinal photoreceptors exosomes miRNAs resolvin D1 VEGFNeovascularization03 medical and health scienceschemistry.chemical_compoundretinal photoreceptors0302 clinical medicinemedicinePharmacology (medical)ReceptorOriginal ResearchPharmacologyChemistrylcsh:RM1-950CorrectionRetinalTransfectionVEGFMicrovesiclesCell biology030104 developmental biologylcsh:Therapeutics. Pharmacology030220 oncology & carcinogenesismiRNAsresolvin D1medicine.symptomIntracellularFrontiers in Pharmacology
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Expression Profile of VEGF-C, VEGF-D, and VEGFR-3 in Different Grades of Endometrial Cancer

2019

Background:Vascular endothelial growth factor (VEGF)-C, -D, and VEGF receptor-3 are proteins characterized as crucial for tumor lymphangiogenesis. It is accompanied by angiogenesis during wound healing, but also in the neoplastic process. The research studies have shown that the lymphatic system plays a key role in the progression of carcinogenesis.Objective:The aim of this study was to evaluate changes in the expression of VEGF-C, VEGF-D and VEGFR-3 in different grades of endometrial cancer (G1-G3).Methods:The study included 45 patients diagnosed with endometrial cancer (G1=17; G2=15; G3=13) and 15 patients without neoplastic changes. The expression of VEGF-C, VEGF-D, and VEGFR-3 was asses…

0301 basic medicineAngiogenesisVascular Endothelial Growth Factor CVascular Endothelial Growth Factor DVEGF-CPharmaceutical ScienceVEGF-Dmedicine.disease_causeMetastasisTranscriptome03 medical and health scienceschemistry.chemical_compound0302 clinical medicinemedicineHumansANOVANeovascularization Pathologicbusiness.industryEndometrial cancerCancerVascular Endothelial Growth Factor Receptor-3medicine.diseaseImmunohistochemistryEndometrial NeoplasmsLymphangiogenesisVEGFR-3lymphangiogenesisVascular endothelial growth factor030104 developmental biologychemistry030220 oncology & carcinogenesisendometrial cancerCancer researchFemaleNeoplasm GradingCarcinogenesisbusinessBiotechnologyCurrent Pharmaceutical Biotechnology
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Cardiotoxic Effects of Anti-VEGFR Tyrosine Kinase Inhibitors

2016

Angiogenesis is a key moment in tumor development and proliferation. Until recently oncologists did not know the mechanisms that were behind this phenomenon, but following the discoveries of Folkman and coworkers, they have gradually created and developed a series of drugs that act against angiogenesis by interacting with molecules belonging to the vascular endothelial growth factor (VEGFs) class and its receptors (VEGFRs) giving rise to anticancer effects. Tyrosine kinase inhibitors (TKIs) are a major class of these new anticancer agents, demonstrating high antitumor activity in a variety of "orphan" neoplasms (such as hepatocellular carcinoma, kidney cancer, sarcomas, etc.). The mechanism…

0301 basic medicineAngiogenesis; Cardio-oncology; Cardiotoxicity; Tyrosine kinase inhibitors; VEGF; VEGF pathway; Medicine (all)Settore MED/06 - Oncologia MedicaAngiogenesisTyrosine kinase inhibitorPharmacology03 medical and health scienceschemistry.chemical_compound0302 clinical medicineVEGF pathwaymedicineReceptorCardiotoxicitybusiness.industryMedicine (all)medicine.diseaseVEGFCardiotoxicityVascular endothelial growth factorAngiogenesiCardio-oncology030104 developmental biologyMechanism of actionchemistry030220 oncology & carcinogenesisHepatocellular carcinomamedicine.symptombusinessKidney cancerTyrosine kinase
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Lyophilized Maqui (Aristotelia chilensis) Berry Induces Browning in the Subcutaneous White Adipose Tissue and Ameliorates the Insulin Resistance in H…

2019

Maqui (Aristotelia Chilensis) berry features a unique profile of anthocyanidins that includes high amounts of delphinidin-3-O-sambubioside-5-O-glucoside and delphinidin-3-O-sambubioside and has shown positive effects on fasting glucose and insulin levels in humans and murine models of type 2 diabetes and obesity. The molecular mechanisms underlying the impact of maqui on the onset and development of the obese phenotype and insulin resistance was investigated in high fat diet-induced obese mice supplemented with a lyophilized maqui berry. Maqui-dietary supplemented animals showed better insulin response and decreased weight gain but also a differential expression of genes involved in de novo…

0301 basic medicineAnthocyaninFGF21Physiologymedicine.medical_treatmentClinical BiochemistryWhite adipose tissueWhite adipose tissueBiochemistryMaqui berryAnthocyanins0302 clinical medicinemaqui berrybiologyChemistryanthocyaninsHigh-fat diethigh-fat dietLipogenesisObesitatmedicine.medical_specialtyRatolins (Animals de laboratori)030209 endocrinology & metabolismfibroblast growth factor 21carbohydrate-responsive element binding protein bArticle03 medical and health sciencesAristotelia chilensisInsulin resistancewhite adipose tissueInternal medicinemedicineObesityCarbohydrate-responsive element-binding proteinMolecular BiologybrowningdelphinidinInsulinlcsh:RM1-950Adipose tissuesCell Biologybiology.organism_classificationmedicine.diseaseTeixit adipós030104 developmental biologyEndocrinologylcsh:Therapeutics. PharmacologyMice (Laboratory animals)AlimentsThermogenesisAntioxidants
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Dynamics and predicted drug response of a gene network linking dedifferentiation with β-catenin dysfunction in hepatocellular carcinoma

2019

Background & Aims Alterations of individual genes variably affect the development of hepatocellular carcinoma (HCC). Thus, we aimed to characterize the function of tumor-promoting genes in the context of gene regulatory networks (GRNs). Methods Using data from The Cancer Genome Atlas, from the LIRI-JP (Liver Cancer – RIKEN, JP project), and from our transcriptomic, transfection and mouse transgenic experiments, we identify a GRN which functionally links LIN28B-dependent dedifferentiation with dysfunction of β-catenin (CTNNB1). We further generated and validated a quantitative mathematical model of the GRN using human cell lines and in vivo expression data. Results We found that LIN28B and C…

0301 basic medicineBeta-cateninCarcinoma HepatocellularHepatocellular carcinomaLIN28BCellGene regulatory networkPrincipal component analysisMice TransgenicBiologyTransfectionTranscriptomeCohort Studies03 medical and health sciencesMice0302 clinical medicineMathematical modelmicroRNAmedicineAnimalsHumansGene Regulatory NetworksCTNNB1Genebeta CateninHepatologySequence Analysis RNALiver NeoplasmsGene regulatory networkRNA-Binding ProteinsHGF/MET pathwayMicroRNAHep G2 CellsHCCSModels TheoreticalPrognosisPersonalized medicinedigestive system diseases030104 developmental biologymedicine.anatomical_structureCancer researchSMARCA4biology.protein030211 gastroenterology & hepatologyTranscriptome
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The cytoprotective protein MANF promotes neuronal survival independently from its role as a GRP78 cofactor

2021

Mesencephalic astrocyte-derived neurotrophic factor (MANF) is an endoplasmic reticulum (ER)-stress-regulated protein exhibiting cytoprotective properties through a poorly understood mechanism in various in vitro and in vivo models of neuronal and non-neuronal damage. Although initially characterized as a secreted neurotrophic factor for midbrain dopamine neurons, MANF has recently gained more interest for its intracellular role in regulating the ER homeostasis, including serving as a cofactor of the chaperone glucose-regulated protein 78 (GRP78). We aimed for a better understanding of the neuroprotective mechanisms of MANF. Here we show for the first time that MANF promotes the survival of …

0301 basic medicineBiFC bimolecular fluorescence complementationMST microscale thermophoresisPDIA1 protein disulfide isomerase family A member 1ApoptosisNEUROTROPHIC FACTOR MANFEndoplasmic ReticulumBiochemistryprotein-protein interactionMiceBimolecular fluorescence complementationUPR unfolded protein responseENDOPLASMIC-RETICULUM STRESSMesencephalonNeurotrophic factorsInsulin-Secreting CellsProtein Interaction MappingBINDINGCOMPREHENSIVE RESOURCEATF6unfolded protein response (UPR)PDIA6 protein disulfide isomerase family A member 6PPIs protein-protein interactionsEndoplasmic Reticulum Chaperone BiPHeat-Shock ProteinsNPTN neuroplastinbiologyChemistryapoptosisunfolded protein responsedopamine neurons3. Good healthCell biologyGDNF glial cell line–derived neurotrophic factorIRE1-ALPHASBD substrate-binding domainendoplasmic reticulum stressMANF mesencephalic astrocyte-derived neurotrophic factorTm tunicamycinneuroprotectionResearch ArticleProtein BindingSignal TransductionGRP78Protein Disulfide-Isomerase FamilyCell SurvivalTH tyrosine hydroxylasePrimary Cell CultureSCG superior cervical ganglionProtein Disulfide-IsomerasesIRE1 inositol-requiring enzyme 1ER-STRESSER endoplasmic reticulum03 medical and health sciencesohjelmoitunut solukuolemaC-MANF C-terminal domain of MANFCSPs chemical shift perturbationsAnimalsHumansHSP70 Heat-Shock ProteinsNerve Growth FactorsNBD nucleotide-binding domainNMR nuclear magnetic resonanceMolecular Biology030102 biochemistry & molecular biologyBIPATF6Dopaminergic NeuronsGene Expression ProfilingBinding proteinneuronal cell deathDISSOCIATIONCell BiologyNEI nucleotide exchange inhibitorEmbryo MammalianadenosiinitrifosfaattiATPhermosolutmesencephalic astrocyte-derived neurotrophic factorprotein–protein interactionPERK protein kinase RNA-like ER kinaseHEK293 Cells030104 developmental biologyGene Expression RegulationChaperone (protein)Tg thapsigarginbiology.proteinUnfolded protein responseAP-MS affinity purification mass spectrometry1182 Biochemistry cell and molecular biologyGFP-SH SH-tagged GFPendoplasmic reticulum stress (ER stress)DA dopaminemesencephalic astrocyte-derived neurotrophic factor (MANF)proteiinitNeuroplastin
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Critical Roles of EGFR family members in breast cancer and breast cancer stem cells: Targets for therapy

2016

The roles of the epidermal growth factor receptor (EGFR) signaling pathway in various cancers including breast, bladder, brain, colorectal, esophageal, gastric, head and neck, hepatocellular, lung, neuroblastoma, ovarian, pancreatic, prostate, renal and other cancers have been keenly investigated since the 1980's. While the receptors and many downstream signaling molecules have been identified and characterized, there is still much to learn about this pathway and how its deregulation can lead to cancer and how it may be differentially regulated in various cell types. Multiple inhibitors to EGFR family members have been developed and many are in clinical use. Current research often focuses o…

0301 basic medicineCA15-3OncologyEGFR HER2 mIRs Cancer Stem Cells Drug Resistance Metastasismedicine.medical_specialtyEGFRDrug ResistancemIRCancer Stem CellBreast NeoplasmsNOMetastasisMetastasis03 medical and health sciences0302 clinical medicineBreast cancerCancer stem cellInternal medicineCancer Stem CellsHER2Drug DiscoverymicroRNAmedicineCancer Stem Cells; Drug Resistance; EGFR; HER2; Metastasis; mIRs; Pharmacology; Drug Discovery3003 Pharmaceutical ScienceAnimalsHumansEpidermal growth factor receptorPharmacologyCancer Stem Cells; Drug Resistance; EGFR; HER2; Metastasis; mIRsmIRsbiologybusiness.industryEGFR HER2 mIRs Cancer Stem Cells Drug Resistance Metastasis.Drug Discovery3003 Pharmaceutical ScienceCancermedicine.disease3. Good healthErbB Receptors030104 developmental biology030220 oncology & carcinogenesisbiology.proteinNeoplastic Stem CellsFemaleStem cellbusinessSignal Transduction
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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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Long Pentraxin 3-Mediated Fibroblast Growth Factor Trapping Impairs Fibrosarcoma Growth

2018

Fibrosarcomas are soft tissue mesenchymal tumors originating from transformed fibroblasts. Fibroblast growth factor-2 (FGF2) and its tyrosine-kinase receptors (FGFRs) play pivotal roles in fibrosarcoma onset and progression, FGF2 being actively produced by fibroblasts in all stages along their malignant transformation to the fibrosarcoma stage. The soluble pattern recognition receptor long pentraxin-3 (PTX3) is an extrinsic oncosuppressor whose expression is reduced in different tumor types, including soft tissue sarcomas, via hypermethylation of its gene promoter. PTX3 interacts with FGF2 and other FGF family members, thus acting as a multi-FGF antagonist able to inhibit FGF-dependent neov…

0301 basic medicineCancer ResearchFGF; FGF-trap; FGFR; fibrosarcoma; long pentraxin-3Fibroblast growth factorlcsh:RC254-282Malignant transformation03 medical and health sciences0302 clinical medicinemedicineFGFFibrosarcomaFibroblastReceptorneoplasmsOriginal ResearchFGF-trapintegumentary systemChemistryFGFRMesenchymal stem cellPTX3medicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens030104 developmental biologymedicine.anatomical_structurelong pentraxin-3OncologyFibroblast growth factor receptor030220 oncology & carcinogenesisCancer researchfibrosarcomaFrontiers in Oncology
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