Search results for "Hypoxia-Inducible Factor 1"

showing 10 items of 67 documents

Hypoxia inducible factor-1alpha inactivation unveils a link between tumor cell metabolism and hypoxia-induced cell death.

2008

Hypoxia and the acquisition of a glycolytic phenotype are intrinsic features of the tumor microenvironment. The hypoxia inducible factor-1alpha (HIF-1alpha) pathway is activated under hypoxic conditions and orchestrates a complex transcriptional program that enhances cell survival. Although the consequences of HIF-1alpha inactivation in cancer cells have been widely investigated, only a few studies have addressed the role of HIF-1alpha in the survival of cancer cells endowed with different glycolytic capacities. In this study, we investigated this aspect in ovarian cancer cells. Hypoxia-induced toxicity was increased in highly glycolytic cells compared with poorly glycolytic cells; it was a…

Programmed cell deathMice SCIDBiologyPathology and Forensic MedicineMiceCell Line TumormedicineAnimalsHumansGene SilencingRNA Small InterferingCell ProliferationOvarian NeoplasmsTumor microenvironmentCell DeathCell growthLentivirusHypoxia (medical)Hypoxia-Inducible Factor 1 alpha SubunitCell HypoxiaCell biologyPhenotypeHypoxia-inducible factorsApoptosisCell cultureCancer cellFemalemedicine.symptomRegular ArticlesThe American journal of pathology
researchProduct

Protein modulation in mouse heart under acute and chronic hypoxia

2011

Exploring cellular mechanisms underlying beneficial and detrimental responses to hypoxia represents the object of the present study. Signaling molecules controlling adaptation to hypoxia (HIF-1α), energy balance (AMPK), mitochondrial biogenesis (PGC-1α), autophagic/apoptotic processes regulation and proteomic dysregulation were assessed. Responses to acute hypoxia (AH) and chronic hypoxia (CH) in mouse heart proteome were detected by 2-D DIGE, mass spectrometry and antigen-antibody reactions. Both in AH and CH, the results indicated a deregulation of proteins related to sarcomere stabilization and muscle contraction. Neither in AH nor in CH the HIF-1α stabilization was observed. In AH, the …

ProteomicsCell signalingProteomeImmunoblottingApoptosisBiologyProtein degradationBiochemistryTwo-Dimensional Difference Gel ElectrophoresisMiceContractile ProteinsHeat shock proteinmedicineAnimalsHypoxiaMolecular BiologyHeat-Shock ProteinsAnimalMyocardiumAutophagyAMPK / Animal proteomics / Apoptosis / Autophagy / Heart / HypoxiaApoptosiProteomicAMPKHeat-Shock ProteinHypoxia (medical)Hypoxia-Inducible Factor 1 alpha SubunitCell biologyGene Expression RegulationMitochondrial biogenesisBiochemistrySpectrometry Mass Matrix-Assisted Laser Desorption-IonizationAdenosylhomocysteinaseContractile Proteinmedicine.symptomEnergy MetabolismPROTEOMICS
researchProduct

Functional regulation of HIF-1α under normoxia--is there more than post-translational regulation?

2011

The hypoxia-inducible factor-1 (HIF-1) is an oxygen-regulated transcriptional activator playing a pivotal role in mammalian physiology and disease pathogenesis, e.g., HIF-1 is indispensable in a broad range of developmental stages in different tumors. Its post-translational regulation via PHDs under the influence of hypoxia is widely investigated and accepted. Different non-hypoxic stimuli such as lipopolysaccharides (LPS), thrombin, and angiotensin II (Ang II), have been proven to enhance HIF-1 levels through activation of regulative mechanisms distinct from protein stabilization. Some of these stimuli specifically regulate HIF-1α at the transcriptional, post-transcriptional, or translatio…

Regulation of gene expressionMammalsHypoxia-Inducible Factor 1PhysiologyClinical BiochemistryCell BiologyHypoxia (medical)BiologyDisease pathogenesisHypoxia-Inducible Factor 1 alpha SubunitAngiotensin IICell biologyOxygenThrombinBiochemistryGene Expression RegulationmedicineAnimalsPost-translational regulationmedicine.symptomProtein stabilizationmedicine.drugJournal of cellular physiology
researchProduct

Short-Time Ocular Ischemia Induces Vascular Endothelial Dysfunction and Ganglion Cell Loss in the Pig Retina

2019

Visual impairment and blindness are often caused by retinal ischemia-reperfusion (I/R) injury. We aimed to characterize a new model of I/R in pigs, in which the intraocular pathways were not manipulated by invasive methods on the ocular system. After 12 min of ischemia followed by 20 h of reperfusion, reactivity of retinal arterioles was measured in vitro by video microscopy. Dihydroethidium (DHE) staining, qPCR, immunohistochemistry, quantification of neurons in the retinal ganglion cell layer, and histological examination was performed. Retinal arterioles of I/R-treated pigs displayed marked attenuation in response to the endothelium-dependent vasodilator, bradykinin, compared to sham-tre…

Retinal Ganglion CellsVascular Endothelial Growth Factor A0301 basic medicinePathologySwineNitric Oxide Synthase Type IIVasodilationendothelial dysfunctionlcsh:Chemistrychemistry.chemical_compound0302 clinical medicineIschemiaEndothelial dysfunctionlcsh:QH301-705.5SpectroscopyGeneral MedicineComputer Science ApplicationsArteriolesmedicine.anatomical_structureRetinal ganglion cellReperfusion InjuryNADPH Oxidase 2medicine.medical_specialtyEndotheliumRetinal ArteryI/R injuryIschemiaretinal arteriolesBradykininRetinal ganglionRetinaArticleCatalysisganglion cell lossInorganic Chemistry03 medical and health sciencesmedicineAnimalsPhysical and Theoretical ChemistryMolecular BiologyRetinabusiness.industryOrganic ChemistryRetinalHypoxia-Inducible Factor 1 alpha Subunitmedicine.disease030104 developmental biologylcsh:Biology (General)lcsh:QD1-999chemistry030221 ophthalmology & optometryEndothelium VascularReactive Oxygen SpeciesbusinessInternational Journal of Molecular Sciences
researchProduct

Inhibition of VEGF expression through blockade of Hif1a and STAT3 signalling mediates the anti-angiogenic effect of melatonin in HepG2 liver cancer c…

2013

Background: Hepatocellular carcinoma (HCC) growth relies on angiogenesis via vascular endothelial growth factor (VEGF) release. Hypoxia within tumour environment leads to intracellular stabilisation of hypoxia inducible factor 1 alpha (Hif1α) and signal transducer and activator of transcription (STAT3). Melatonin induces apoptosis in HCC, and shows anti-angiogenic features in several tumours. In this study, we used human HepG2 liver cancer cells as an in vitro model to investigate the anti-angiogenic effects of melatonin. Methods: HepG2 cells were treated with melatonin under normoxic or CoCl2-induced hypoxia. Gene expression was analysed by RT–qPCR and western blot. Melatonin-induced anti-…

STAT3 Transcription FactorTranscriptional ActivationVascular Endothelial Growth Factor ACancer ResearchCarcinoma HepatocellularTranscription GeneticAngiogenesisAngiogenesis InhibitorsApoptosismelatoninP300-CBP Transcription FactorsHif1αBiologyMelatoninSTAT3chemistry.chemical_compoundHypoxia-Inducible Factor 1-AlphamedicineHuman Umbilical Vein Endothelial CellsHumansp300-CBP Transcription FactorsSTAT3Promoter Regions GeneticTube formationNeovascularization PathologicLiver NeoplasmsCobaltHep G2 Cellshepatocellular carcinomaHypoxia-Inducible Factor 1 alpha SubunitVEGFCell Hypoxiadigestive system diseasesCyclic S-OxidesVascular endothelial growth factorGene Expression Regulation NeoplasticVascular endothelial growth factor AOncologychemistryCancer researchbiology.proteinTranslational Therapeuticsmedicine.drugSignal Transduction
researchProduct

miR-20b modulates VEGF expression by targeting HIF-1 alpha and STAT3 in MCF-7 breast cancer cells.

2010

MicroRNAs (miRNAs) are small non-coding RNAs that regulate the expression of different genes, including genes involved in cancer progression. A functional link between hypoxia, a key feature of the tumor microenvironment, and miRNA expression has been documented. We investigated whether and how miR-20b can regulate the expression of vascular endothelial growth factor (VEGF) in MCF-7 breast cancer cells under normoxic and hypoxia-mimicking conditions (CoCl(2) exposure). Using immunoblotting, ELISA, and quantitative real-time PCR, we demonstrated that miR-20b decreased VEGF protein levels at 4 and 24 h following CoCl(2) treatment, and VEGF mRNA at 4 h of treatment. In addition, miR-20b reduce…

STAT3 Transcription FactorVascular Endothelial Growth Factor ATime FactorsPhysiologySettore MED/06 - Oncologia MedicaClinical BiochemistryDown-RegulationBreast NeoplasmsBiologyTransfectionchemistry.chemical_compoundmir20b VEGFCell Line TumormicroRNAHumansSTAT3Promoter Regions GeneticG alpha subunitRegulation of gene expressionTumor microenvironmentBinding SitesCell BiologyTransfectionCobaltHypoxia-Inducible Factor 1 alpha SubunitMolecular biologyCell HypoxiaVascular endothelial growth factorGene Expression Regulation NeoplasticMicroRNAsHIF1Achemistrybiology.proteinFemaleRNA InterferenceSignal TransductionJournal of cellular physiology
researchProduct

Hif1 Is a Component of Yeast Histone Acetyltransferase B, a Complex Mainly Localized in the Nucleus

2004

Hat1 is the catalytic subunit of the only type B histone acetyltransferase known (HAT-B). The enzyme specifically acetylates lysine 12, and to a lesser extent lysine 5, of free, non-chromatin-bound histone H4. The complex is usually isolated with cytosolic fractions and is thought to be involved in chromatin assembly. The Saccharomyces cerevisiae HAT-B complex also contains Hat2, a protein stimulating Hat1 catalytic activity. We have now identified by two-hybrid experiments Hif1 as both a Hat1- and a histone H4-interacting protein. These interactions were dependent on HAT2, indicating a mediating role for Hat2. Biochemical fractionation and co-immunoprecipitation assays demonstrated that Hi…

Saccharomyces cerevisiae ProteinsbiologyNuclear ProteinsAcetylationSaccharomyces cerevisiaeCell BiologyHistone acetyltransferaseTelomereBiochemistryDNA-Binding ProteinsHistonesHistone H4HistoneBiochemistryAcetyltransferasesHistone methyltransferaseHistone H2Abiology.proteinHistone codeHypoxia-Inducible Factor 1Histone octamerHAT1Molecular BiologyHistone AcetyltransferasesTranscription FactorsJournal of Biological Chemistry
researchProduct

Cholesterol Starvation and Hypoxia Activate the FVII Gene via the SREBP1-GILZ Pathway in Ovarian Cancer Cells to Produce Procoagulant Microvesicles

2019

AbstractInteraction between the transcription factors, hypoxia-inducible factor (HIF1α and HIF2α) and Sp1, mediates hypoxia-driven expression of FVII gene encoding coagulation factor VII (fVII) in ovarian clear cell carcinoma (CCC) cells. This mechanism is synergistically enhanced in response to serum starvation, a condition possibly associated with tumor hypoxia. This transcriptional response potentially results in venous thromboembolism, a common complication in cancer patients by producing procoagulant extracellular vesicles (EVs). However, which deficient serum factors are responsible for this characteristic transcriptional mechanism is unknown. Here, we report that cholesterol deficien…

Serum0301 basic medicineLeucine zipper030204 cardiovascular system & hematologyMice03 medical and health sciences0302 clinical medicineCell-Derived MicroparticlesCell Line Tumorhemic and lymphatic diseasesAnimalsHumansHypoxiaTranscription factorOvarian NeoplasmsTumor hypoxiaCoagulantsChemistryHematologyFactor VIIChromatin Assembly and DisassemblyHypoxia-Inducible Factor 1 alpha SubunitXenograft Model Antitumor AssaysMicrovesiclesChromatinCell biologySterol regulatory element-binding proteinCholesterol030104 developmental biologyFemaleSignal transductionSterol Regulatory Element Binding Protein 1Chromatin immunoprecipitationSignal TransductionTranscription FactorsThrombosis and Haemostasis
researchProduct

Long Non Coding RNA H19: A New Player in Hypoxia-Induced Multiple Myeloma Cell Dissemination

2019

The long non-coding RNA H19 (lncH19) is broadly transcribed in the first stage of development and silenced in most cells of an adult organism

Stromal cellCellHIF-1αBiologyModels BiologicalCatalysisArticleInorganic Chemistrylcsh:ChemistryChemokine receptorWestern blotSettore BIO/13 - Biologia ApplicataCell Line TumormedicineCell AdhesionGene silencingHumansHIF-1 alfaPhysical and Theoretical ChemistryMolecular Biologylcsh:QH301-705.5Spectroscopymedicine.diagnostic_testCell growthhypoxiaOrganic ChemistryGeneral MedicineHypoxia (medical)Hypoxia-Inducible Factor 1 alpha Subunitfemale genital diseases and pregnancy complicationsComputer Science ApplicationsCell biologyGene Expression Regulation Neoplasticmultiple myelomamedicine.anatomical_structurelcsh:Biology (General)lcsh:QD1-999Cell cultureembryonic structuresRNA Long Noncodingmedicine.symptomStromal Cellslong non-coding RNA H19 (lncH19)International Journal of Molecular Sciences
researchProduct

Recruitment of HIF-1α and HIF-2α to common target genes is differentially regulated in neuroblastoma: HIF-2α promotes an aggressive phenotype

2006

In neuroblastoma specimens, HIF-2alpha but not HIF-1alpha is strongly expressed in well-vascularized areas. In vitro, HIF-2alpha protein was stabilized at 5% O2 (resembling end capillary oxygen conditions) and, in contrast to the low HIF-1alpha activity at this oxygen level, actively transcribed genes like VEGF. Under hypoxia (1% O2), HIF-1alpha was transiently stabilized and primarily mediated acute responses, whereas HIF-2alpha protein gradually accumulated and governed prolonged hypoxic gene activation. Knockdown of HIF-2alpha reduced growth of neuroblastoma tumors in athymic mice. Furthermore, high HIF-2alpha protein levels were correlated with advanced clinical stage and high VEGF expr…

Transcriptional ActivationCancer ResearchProcollagen-Proline DioxygenaseAggressive phenotypeCELLCYCLEBiologyMiceNeuroblastomaNeuroblastomaBasic Helix-Loop-Helix Transcription FactorsTumor Cells CulturedmedicineAnimalsHumansRNA MessengerChildHypoxiaGeneOligonucleotide Array Sequence AnalysisRegulation of gene expressionGene knockdownGene Expression ProfilingCell BiologyCell cycleHypoxia (medical)Hypoxia-Inducible Factor 1 alpha Subunitmedicine.diseaseIn vitroGene Expression Regulation NeoplasticOxygenPhenotypeOncologyImmunologyCancer researchFemalemedicine.symptomNeoplasm TransplantationCancer Cell
researchProduct