Search results for "EGFR signaling"

showing 4 items of 4 documents

Loss of PHD3 allows tumours to overcome hypoxic growth inhibition and sustain proliferation through EGFR

2014

Solid tumours are exposed to microenvironmental factors such as hypoxia that normally inhibit cell growth. However, tumour cells are capable of counteracting these signals through mechanisms that are largely unknown. Here we show that the prolyl hydroxylase PHD3 restrains tumour growth in response to microenvironmental cues through the control of EGFR. PHD3 silencing in human gliomas or genetic deletion in a murine high-grade astrocytoma model markedly promotes tumour growth and the ability of tumours to continue growing under unfavourable conditions. The growth-suppressive function of PHD3 is independent of the established PHD3 targets HIF and NF-κB and its hydroxylase activity. Instead, l…

MaleColorectal cancerAngiogenesisProcollagen-Proline DioxygenaseGeneral Physics and AstronomyApoptosisGrowth inhibitoryBiologyArticleGeneral Biochemistry Genetics and Molecular BiologyHypoxia-Inducible Factor-Proline DioxygenasesGene Knockout Techniqueschemistry.chemical_compoundCell Line TumormedicineAnimalsHumansEgfr signalingHypoxiaCell ProliferationMice KnockoutMultidisciplinaryCell growthGeneral ChemistryHypoxia (medical)Hypoxia-Inducible Factor 1 alpha Subunitmedicine.diseaseMolecular biologyErbB ReceptorsOxygenchemistryApoptosisCancer researchFemalemedicine.symptomGrowth inhibitionGlioblastomaNature Communications
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MiR-33a Controls hMSCS Osteoblast Commitment Modulating the Yap/Taz Expression Through EGFR Signaling Regulation

2019

Mesenchymal stromal cells (hMSCs) display a pleiotropic function in bone regeneration. The signaling involved in osteoblast commitment is still not completely understood, and that determines the failure of current therapies being used. In our recent studies, we identified two miRNAs as regulators of hMSCs osteoblast differentiation driving hypoxia signaling and cytoskeletal reorganization. Other signalings involved in this process are epithelial to mesenchymal transition (EMT) and epidermal growth factor receptor (EGFR) signalings through the regulation of Yes-associated protein (YAP)/PDZ-binding motif (TAZ) expression. In the current study, we investigated the role of miR-33a family as a (…

epithelial mesenchymal transitionregenerative medicinePDZ DomainsCell CommunicationArticlemicroRNAmedicineHumansEpidermal growth factor receptorEpithelial–mesenchymal transitionBone regenerationCells CulturedEGFR inhibitorsAdaptor Proteins Signal TransducingOsteoblastsmicroRNAbiologyMesenchymal stem cellComputational BiologyOsteoblastMesenchymal Stem CellsYAP-Signaling ProteinsGeneral MedicinePhenotypeCell biologymicroRNAsErbB Receptorsmedicine.anatomical_structureTranscriptional Coactivator with PDZ-Binding Motif Proteinsmesenchymal stromal cellbiology.proteinTrans-Activatorsmesenchymal stromal cellsEGFR signalingSignal TransductionTranscription FactorsCells
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71P Exosomes isolated in plasma of non-small cell lung cancer patients contain microRNA related to the EGFR pathway: Proof of concept

2016

0301 basic medicinePulmonary and Respiratory Medicinebusiness.industrymedicine.diseaseMicrovesiclesCell biology03 medical and health sciences030104 developmental biology0302 clinical medicineOncology030220 oncology & carcinogenesismicroRNAmedicineEgfr signalingNon small cellLung cancerbusinessJournal of Thoracic Oncology
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Additive effects of cherlerythrine chloride combination with erlotinib in human non-small cell lung cancer cells

2017

Several studies implicate that lung cancer progression is governed by the interaction between epidermal growth factor receptor (EGFR) signaling and protein kinase C (PKC) pathways. Combined the targeting of EGFR and PKC may have an additive or synergistic effects in lung cancer treatment. The aim of this study is to explore the potential utility by inhibiting these two pathways with the combination of erlotinib and chelerythrine chloride in non-small cell lung cancer (NSCLC) cell lines. The erlotinib-less sensitive cell lines SK-MES-1 and A549 were treated with erlotinib or chelerythrine by themselves or in combination with each other. The cell viability, clonogenic survival, cell migration…

Male0301 basic medicineOncologyCell signalingLung NeoplasmsCancer Treatmentlcsh:MedicineApoptosisMice SCIDSignal transductionLung and Intrathoracic TumorsMicechemistry.chemical_compoundMice Inbred NODCarcinoma Non-Small-Cell LungMedicine and Health SciencesEpidermal growth factor receptorPhosphorylationlcsh:ScienceErlotinib HydrochlorideMultidisciplinaryCell DeathbiologyPharmaceuticsChemistrySignaling cascadesFlow CytometryErbB ReceptorsCell MotilityOncologyCell ProcessesDrug Therapy CombinationErlotinibSignal transductionEGFR signalingResearch Articlemedicine.drugmedicine.medical_specialtyMAPK signaling cascadesCell MigrationErlotinib Hydrochloride03 medical and health sciencesDrug TherapyCell Line TumorInternal medicinemedicineAnimalsHumansViability assayLung cancerBenzophenanthridineslcsh:RCancers and NeoplasmsBiology and Life SciencesCell Biologymedicine.diseaseXenograft Model Antitumor AssaysNon-Small Cell Lung Cancerrespiratory tract diseases030104 developmental biologyChelerythrineApoptosisCancer researchbiology.proteinlcsh:QDevelopmental BiologyPLOS ONE
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