Search results for "Hypoxia-Inducible Factor-Proline Dioxygenases"

showing 5 items of 5 documents

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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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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Identification of a novel recurrent 1q42.2-1qter deletion in high risk MYCN single copy 11q deleted neuroblastomas

2012

Neuroblastoma is an aggressive embryonal tumor that accounts for similar to 15% of childhood cancer deaths. Hitherto, despite the availability of comprehensive genomic data on DNA copy number changes in neuroblastoma, relatively little is known about the genes driving neuroblastoma tumorigenesis. In this study, high resolution array comparative genome hybridization (CGH) was performed on 188 primary neuroblastoma tumors and 33 neuroblastoma cell lines to search for previously undetected recurrent DNA copy number gains and losses. A new recurrent distal chromosome 1q deletion (del(1)(q42.2qter)) was detected in seven cases. Further analysis of available array CGH datasets revealed 13 additio…

Neuroblastoma/geneticsCancer ResearchProcollagen-Proline DioxygenaseMedizinGene Dosagecomparative genomic hybridizationBiologymedicine.disease_causeGene dosageN-Myc Proto-Oncogene ProteinFumarate HydrataseHypoxia-Inducible Factor-Proline DioxygenasesNeuroblastomaProcollagen-Proline Dioxygenase/geneticsCell Line TumorNeuroblastomamedicineHumansFumarate Hydratase/geneticsGeneOncogene ProteinsGeneticsN-Myc Proto-Oncogene ProteinChromosomes Human Pair 11BreakpointNuclear ProteinsChromosomemedicine.diseaseOncogene Proteins/geneticsNuclear Proteins/geneticsOncologyChromosome DeletionCarcinogenesisComparative genomic hybridization
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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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Role of reactive oxygen species in the regulation of HIF-1 by prolyl hydroxylase 2 under mild hypoxia

2012

The function and survival of eukaryotic cells depends on a constant and sufficient oxygen supply. Cells recognize and respond to hypoxia by accumulation of the transcription factor hypoxia-inducible factor 1 (HIF-1), composed of an oxygen-sensitive HIF-1α and a constitutive HIF-1β subunit. Besides physiology, HIF-1 induction is involved in major pathological processes such as cardiovascular disease, inflammation and cancer, which are associated with the formation of reactive oxygen species (ROS). ROS have been reported to affect HIF-1 activity but the role for ROS in regulating HIF-1 has not been definitely settled. In order to shed light on the redox-regulation of HIF-1 by ROS, we studied …

Transcriptional ActivationProcollagen-Proline DioxygenaseMedizinBiologyTransfectionBiochemistryHypoxia-Inducible Factor-Proline DioxygenasesTransactivationCell Line TumormedicineHumansRNA Small InterferingTranscription factorchemistry.chemical_classificationRegulation of gene expressionReactive oxygen speciesGene knockdownGeneral MedicineTransfectionHydrogen PeroxideHypoxia (medical)Cell HypoxiaCell biologyHypoxia-inducible factorschemistryBiochemistryHypoxia-Inducible Factor 1medicine.symptomReactive Oxygen SpeciesOxidation-Reduction
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