Search results for "ErbB Receptor"

showing 10 items of 167 documents

Aclidinium inhibits cholinergic and tobacco smoke-induced MUC5AC in human airways.

2010

Mucus hypersecretion and mucin MUC5AC overexpression are pathological features of chronic obstructive pulmonary disease (COPD). This study examines the inhibitory effect of aclidinium, a new long-acting muscarinic antagonist, on MUC5AC expression in human airway epithelial cells. MUC5AC mRNA (RT-PCR) and protein expression (ELISA and immunohistochemistry) were studied in human bronchial tissue and differentiated human airway epithelial cells activated with carbachol (100 μM) or cigarette smoke extract in the absence or presence of aclidinium. Carbachol increased MUC5AC mRNA and protein expression in human bronchus and cultured epithelial cells. Aclidinium inhibited the carbachol-induced MUC…

Pulmonary and Respiratory MedicineMAPK/ERK pathwaymedicine.medical_specialtyCarbacholRespiratory SystemMuscarinic AntagonistsPharmacologyMucin 5ACPulmonary Disease Chronic ObstructiveDownregulation and upregulationInternal medicinemedicineHumansRNA Small InterferingCells CulturedBronchusbusiness.industryMucinSmokingEpithelial Cellsrespiratory systemMucusEpitheliumErbB ReceptorsEndocrinologymedicine.anatomical_structureCarbacholMitogen-Activated Protein KinasesbusinessTyrosine kinasemedicine.drugTropanesThe European respiratory journal
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Caveolin-1, breast cancer and ionizing radiation

2015

Breast cancer (BC) recovery has increased in recent years thanks to efforts of Omics-based research in this field. However, despite the important results obtained, BC remains a complex multifactorial pathology that is difficult to treat appropriately. Caveolin-1 (CAV1), the basic constituent protein of specialized plasma membrane invaginations called caveolae, is emerging as a potential therapeutic biomarker in BC. This factor may modulate BC response to chemotherapy and radiation therapy. In addition, recent reports describe the key role of CAV1 during cell response to oxidative stress. The aim of the present review was to describe the biological roles of CAV1 in BC considering its contras…

RadiotherapyAnimalCAV1; biomarker; breast cancer; ionizing radiation; review; Animals; Biomarkers Tumor; Breast Neoplasms; Caveolin 1; Cell Transformation Neoplastic; Female; Gene Expression Regulation Neoplastic; Humans; Molecular Targeted Therapy; Radiotherapy; Receptor Epidermal Growth Factor; Radiation IonizingCaveolin 1reviewBreast NeoplasmsErbB ReceptorsGene Expression Regulation Neoplasticbreast cancerCell Transformation NeoplasticCAV1Radiation IonizingBiomarkers TumorAnimalsHumansbiomarkerFemaleMolecular Targeted TherapyReceptor Epidermal Growth Factorionizing radiationBreast NeoplasmHuman
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Erbb2 regulates neuromuscular synapse formation and is essential for muscle spindle development

2003

Neuregulins and their Erbb receptors have been implicated in neuromuscular synapse formation by regulating gene expression in subsynaptic nuclei. To analyze the function of Erbb2 in this process, we have inactivated the Erbb2 gene in developing muscle fibers by Cre/Lox-mediated gene ablation. Neuromuscular synapses form in the mutant mice, but the synapses are less efficient and contain reduced levels of acetylcholine receptors. Surprisingly, the mutant mice also show proprioceptive defects caused by abnormal muscle spindle development. Sensory Ia afferent neurons establish initial contact with Erbb2-deficient myotubes. However, functional spindles never develop. Taken together, our data su…

Receptor ErbB-2Muscle spindleNeuromuscular JunctionMice TransgenicBiologySynaptic TransmissionNeuromuscular junctionSynapseMiceErbB ReceptorsmedicineAnimalsHumansMuscle SkeletalPromoter Regions Geneticskin and connective tissue diseasesMuscle SpindlesMolecular BiologyAcetylcholine receptorMice KnockoutAfferent PathwaysMyogenesisGenes erbB-2ActinsMice Mutant StrainsCell biologyMice Inbred C57BLmedicine.anatomical_structureSilent synapseNeuregulinSignal TransductionDevelopmental BiologyDevelopment
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SAHA/TRAIL combination induces detachment and anoikis of MDA-MB231 and MCF-7 breast cancer cells

2012

Abstract SAHA, an inhibitor of histone deacetylase activity, has been shown to sensitize tumor cells to apoptosis induced by TRAIL, a member of TNF-family. In this paper we investigated the effect of SAHA/TRAIL combination in two breast cancer cell lines, the ERα−positive MCF-7 and the ERα−negative MDA-MB231. Treatment of MDA-MB231 and MCF-7 cells with SAHA in combination with TRAIL caused detachment of cells followed by anoikis, a form of apoptosis which occurs after cell detachment, while treatment with SAHA or TRAIL alone did not produce these effects. The effects were more evident in MDA-MB231 cells, which were chosen for ascertaining the mechanism of SAHA/TRAIL action. Our results show…

Recombinant Fusion ProteinsCellCASP8 and FADD-Like Apoptosis Regulating ProteinAntineoplastic AgentsBreast NeoplasmsHydroxamic AcidsCleavage (embryo)BiochemistryTNF-Related Apoptosis-Inducing LigandCell Line TumorProto-Oncogene ProteinsSettore BIO/10 - BiochimicaAntineoplastic Combined Chemotherapy ProtocolsCell AdhesionmedicineSAHA TRAIL Anoikis EGFR FAK BimELHumansAnoikisskin and connective tissue diseasesMda mb231VorinostatBcl-2-Like Protein 11ChemistryMembrane ProteinsGeneral MedicineAnoikisErbB ReceptorsGene Expression Regulation Neoplasticmedicine.anatomical_structureMCF-7ApoptosisCaspasesFocal Adhesion Kinase 1ImmunologyCancer researchPhosphorylationFemaleHistone deacetylase activityApoptosis Regulatory ProteinsSignal Transduction
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PHD3 regulates EGFR internalization and signalling in tumours

2014

Tumours exploit their hypoxic microenvironment to induce a more aggressive phenotype, while curtailing the growth-inhibitory effects of hypoxia through mechanisms that are poorly understood. The prolyl hydroxylase PHD3 is regulated by hypoxia and plays an important role in tumour progression. Here we identify PHD3 as a central regulator of epidermal growth factor receptor (EGFR) activity through the control of EGFR internalization to restrain tumour growth. PHD3 controls EGFR activity by acting as a scaffolding protein that associates with the endocytic adaptor Eps15 and promotes the internalization of EGFR. In consequence, loss of PHD3 in tumour cells suppresses EGFR internalization and hy…

Scaffold proteinmedia_common.quotation_subjectEndocytic cycleRegulatorGeneral Physics and AstronomyGeneral Biochemistry Genetics and Molecular BiologyHypoxia-Inducible Factor-Proline DioxygenasesCell Line TumorNeoplasmsmedicineHumansEpidermal growth factor receptorInternalizationmedia_commonCell ProliferationMultidisciplinarybiologyCell growthChemistryGeneral ChemistryHypoxia (medical)EndocytosisCell biologyErbB ReceptorsGene Expression Regulation NeoplasticAdaptor Proteins Vesicular TransportSignallingbiology.proteinmedicine.symptomProtein BindingSignal Transduction
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The role of targeted therapy for gastrointestinal tumors

2014

Abstract: Many targeted drugs have been studied to target the molecular pathways involved in the development of gastrointestinal cancers. Anti-VEGF, anti-EGFR agents, and recently also multi-kinase inhibitor regorafenib, have already been available for the treatment of metastatic colorectal cancer patients. To date, Her-2 positive, gastric cancer patients, are also treated with trastuzumab, while the multi-targeted inhibitor, sorafenib, represents the standard treatment for hepatocellular carcinoma patients. Finally, sunitinib and everolimus, have been approved for the treatment of the neuroendocrine gastroenteropancreatic tumors. Actually a great number of further drugs are under preclinic…

SorafenibOncologyVascular Endothelial Growth Factor Amedicine.medical_specialtyReceptor ErbB-2Hepatocellular carcinomaSettore MED/06 - Oncologia Medicamedicine.medical_treatmentAntineoplastic AgentsNeuroendocrine tumorsTargeted therapyTargeted therapychemistry.chemical_compoundNeuroendocrine tumorTrastuzumabInternal medicineRegorafenibmedicineHumansGastrointestinal tumorsMolecular Targeted TherapyProtein Kinase InhibitorsGastrointestinal NeoplasmsEverolimusHepatologySunitinibbusiness.industryColorectal cancer; Gastric cancer; Gastrointestinal tumors; Hepatocellular carcinoma; Neuroendocrine tumors; Targeted therapy; Hepatology; GastroenterologyGastrointestinal tumorGastroenterologyCancermedicine.diseaseColorectal cancerErbB ReceptorsReceptors Vascular Endothelial Growth FactorchemistryHuman medicineNeuroendocrine tumorsbusinessGastric cancermedicine.drug
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Epigenetic activation of a cryptic TBC1D16 transcript enhances melanoma progression by targeting EGFR

2015

Metastasis is respoMetastasis is responsible for most cancer-related deaths, and, among common tumor types, melanoma is one with great potential to metastasize. Here we study the contribution of epigenetic changes to the dissemination process by analyzing the changes that occur at the DNA methylation level between primary cancer cells and metastases. We found a hypomethylation event that reactivates a cryptic transcript of the Rab GTPase activating protein TBC1D16 (TBC1D16-47 kDa; referred to hereafter as TBC1D16-47KD) to be a characteristic feature of the metastatic cascade. This short isoform of TBC1D16 exacerbates melanoma growth and metastasis both in vitro and in vivo. By combining imm…

Transcriptional ActivationGTPase-activating proteinImmunoprecipitationMice NudeEditorials: Cell Cycle FeaturesBiologyBioinformaticsMethylationGeneral Biochemistry Genetics and Molecular BiologyEpigenesis GeneticMetastasisMetastasisEpigènesiMetàstasiCell Line TumormedicineAnimalsImmunoprecipitationProtein IsoformsRNA MessengerEpigeneticsNeoplasm MetastasisRNA Small InterferingPromoter Regions GeneticProteïnes supressores de tumorsProtein Kinase InhibitorsMelanomaMelanomaGTPase-Activating ProteinsGeneral MedicineMethylationDNA MethylationPrognosismedicine.diseaseTumor suppressor proteinErbB ReceptorsMolecular WeightTreatment Outcomerab GTP-Binding ProteinsDNA methylationDisease ProgressionCancer researchRabMetilacióProtein BindingSignal TransductionEpigenesisNature Medicine
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Interactions between cholinergic and fibroblast growth factor receptors in brain trophism and plasticity

2014

Acetylcholine, acting on both nicotinic receptors (nAChRs) and muscarinic receptors (mAChRs), plays a role in the regulation of synaptic plasticity, being involved in the regulation of cellular processes and cognitive functions, such as learning, memory and attention. Recently, G protein coupled receptors (GPCRs), including mAChRs, have been reported to transactivate tyrosine-kinase receptors (RTK), such as epidermal growth factor receptor (EGFR), and initiate their intracellular signaling. In this minireview we have first analysed the RTK transactivation mechanisms, involving cholinergic receptors, and thereafter the interplay between AChR and neurotrophic factor systems built up by FGF2 a…

Transcriptional Activationmedicine.medical_specialtyClass C GPCRG protein coupled receptorBiologyCholinergic AgonistsBiochemistrySynaptic plasticityTransactivationNicotinic receptorNeurotrophic factorsInternal medicinemedicineAnimalsHumansReceptors CholinergicProtein Interaction MapsReceptorMolecular BiologyG protein-coupled receptorTransactivationNeuronal PlasticityFibroblast growth factor receptor 1Muscarinic receptorBrainReceptor Protein-Tyrosine KinasesCell BiologyGeneral MedicineReceptors Fibroblast Growth FactorErbB ReceptorsEndocrinologyFGFR1Fibroblast growth factor receptorFGFR1; G protein coupled receptor; Muscarinic receptors; Nicotinic receptors; Receptor-receptor interaction; Synaptic plasticity; Transactivation; Tyrosine-kinase receptorsSignal transductionTyrosine-kinase receptorsNeuroscienceReceptor-receptor interactionSignal Transduction
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Endothelin-1-Mediated Drug Resistance in EGFR-Mutant Non-Small Cell Lung Carcinoma.

2020

Abstract Progression on therapy in non-small cell lung carcinoma (NSCLC) is often evaluated radiographically, however, image-based evaluation of said therapies may not distinguish disease progression due to intrinsic tumor drug resistance or inefficient tumor penetration of the drugs. Here we report that the inhibition of mutated EGFR promotes the secretion of a potent vasoconstrictor, endothelin-1 (EDN1), which continues to increase as the cells become resistant with a mesenchymal phenotype. As EDN1 and its receptor (EDNR) is linked to cancer progression, EDNR-antagonists have been evaluated in several clinical trials with disappointing results. These trials were based on a hypothesis that…

Vascular Endothelial Growth Factor ACancer ResearchLung NeoplasmsAmbrisentanOncology and CarcinogenesisDrug ResistanceBiological AvailabilityAntineoplastic AgentsDrug resistanceCell LineMiceErlotinib HydrochlorideGefitinibIn vivomedicineAnimalsHumansOncology & CarcinogenesisNon-Small-Cell LungProtein Kinase InhibitorsLungCancerTumor microenvironmentTumorEndothelin-1business.industryCarcinomaLung CancerCancerEvaluation of treatments and therapeutic interventionsGefitinibmedicine.diseaseEndothelin 1Xenograft Model Antitumor AssaysErbB ReceptorsOncologyVasoconstriction5.1 Pharmaceuticals6.1 PharmaceuticalsCancer cellMutationCancer researchNeoplasmDevelopment of treatments and therapeutic interventionsbusinessmedicine.drug
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Predicting efficacy and toxicity in the era of targeted therapy: focus on anti-EGFR and anti-VEGF molecules

2011

The treatment of solid malignancies includes various target drugs, such as monoclonal antibodies and tyrosine kinase inhibitors, which exert their effect alone or in combination with chemotherapy. The main part of these molecules have a target on proteins of EGFR and VEGF pathways. The particular toxicity profile and the financial impact, deriving from the application of these agents in cancer treatment, prompted a lot of researches to define predictive factors of their efficacy. Various biomarker were identified among the components of the targeted pathways. However just few studies allowed to identify specific factors to predict the toxicity of these drugs. In this review EGFR and VEGF-re…

Vascular Endothelial Growth Factor Amedicine.drug_classSettore MED/06 - Oncologia Medicamedicine.medical_treatmentClinical BiochemistryAngiogenesis InhibitorsAntineoplastic AgentsPharmacologyMonoclonal antibodyTargeted therapyAntineoplastic AgentNeoplasmsProtein-Tyrosine KinasemedicineHumansAngiogenesis Inhibitors; Antibodies Monoclonal; Antineoplastic Agents; Humans; Neoplasms; Protein-Tyrosine Kinases; Receptor Epidermal Growth Factor; Treatment Outcome; Vascular Endothelial Growth Factor ATarget therapyPharmacologyAnti vegfChemotherapybusiness.industryAntibodies MonoclonalProtein-Tyrosine KinasesErbB ReceptorsTreatment OutcomeToxicityCancer researchBiomarker (medicine)NeoplasmReceptor Epidermal Growth FactorbusinessTyrosine kinaseAngiogenesis InhibitorHuman
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