Search results for "Inducible"

showing 10 items of 111 documents

Hypoxia and Aggressive Tumor Phenotype: Implications for Therapy and Prognosis

2008

Abstract Tumor hypoxia, mostly resulting from poor perfusion and anemia, is one of the key factors in inducing the development of cell clones with an aggressive and treatment-resistant phenotype that leads to rapid progression and poor prognosis. Studies in patients with solid tumors suggest that there is a range of hemoglobin (Hb) concentrations that is optimum for tumor oxygenation. When used to achieve an Hb level within this range, erythropoiesis-stimulating agents (ESAs) can be expected to increase tumor oxygenation, and this may favorably influence sensitivity to treatment as well as quality of life. There is no robust evidence that ESAs, when used as indicated, have a negative effect…

OncologyCancer Researchmedicine.medical_specialtyPathologyAnemiaCellHemoglobinsNeoplasmsInternal medicinemedicineHumansErythropoietinCell ProliferationTumor hypoxiabusiness.industryAnemiaCell DifferentiationHypoxia (medical)Tumor OxygenationHypoxia-Inducible Factor 1 alpha Subunitmedicine.diseasePhenotypeCell HypoxiaRecombinant ProteinsOxygenCell Transformation Neoplasticmedicine.anatomical_structureOncologyHematinicsHemoglobinmedicine.symptombusinessPerfusionThe Oncologist
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MCC1019, a selective inhibitor of the Polo-box domain of Polo-like kinase 1 as novel, potent anticancer candidate

2019

Polo-like kinase (PLK1) has been identified as a potential target for cancer treatment. Although a number of small molecules have been investigated as PLK1 inhibitors, many of which showed limited selectivity. PLK1 harbors a regulatory domain, the Polo box domain (PBD), which has a key regulatory function for kinase activity and substrate recognition. We report on 3-bromomethyl-benzofuran-2-carboxylic acid ethyl ester (designated: MCC1019) as selective PLK1 inhibitor targeting PLK1 PBD. Cytotoxicity and fluorescence polarization-based screening were applied to a library of 1162 drug-like compounds to identify potential inhibitors of PLK1 PBD. The activity of compound MC1019 against the PLK1…

PBD Polo box domainMTD maximal tolerance doseCDC25 cell division cycle 25HIF-1α hypoxia-inducible factor 1 αMST microscale thermophoresisIC50 50% inhibition concentrationMFP M phase promoting factorPARP-1 poly(ADP-ribose) polymerase-10302 clinical medicineFOXO forkhead box ONec-1 necrostatin 1CDC2 cell division cycle protein 2 homologGeneral Pharmacology Toxicology and PharmaceuticsMitotic catastropheCDK cyclin-dependent kinase0303 health sciencesChemistryPolo-like kinaseMono-targeted therapyCell cycleBUBR1 budding uninhibited by benzimidazole-related 1Polo box domain030220 oncology & carcinogenesisPLK1 Polo-like kinaseNecroptosisSpindle damagePLK1IHC immunohistochemistryOriginal articleNecroptosisCell cyclePLK1APC/C anaphase-promoting complex/cyclosomePLK3ABC avidin-biotin complexPI propidium iodide03 medical and health sciencesFBS fetal bovine serumPDB Protein Data BankKd the dissociation constantKinase activity030304 developmental biologyAkt/PKB signaling pathwayCell growthlcsh:RM1-950LC3 light chain 3lcsh:Therapeutics. PharmacologyCancer researchDAPKs death-associated protein kinase3-MA 3-methyladenineDAPI 4′6-diamidino-2-phenylindoleSAC spindle assembly checkpointActa Pharmaceutica Sinica B
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Nitric oxide, derived from inducible nitric oxide synthase, decreases hypoxia inducible factor-1α in macrophages during aspirin-induced mesenteric in…

2010

Background and purpose:  Nitric oxide (NO) modulates expression of hypoxia inducible factor-1 (HIF-1), a transcription factor regulating function of myeloid cells. Here, we have assessed the role played by NO, formed by inducible NOS (iNOS), in the inflammation induced by aspirin in the gut, by modulating HIF-1 activity. Experimental approach:  The role of iNOS-derived NO on leucocyte–endothelial interactions induced by aspirin was evaluated by intravital microscopy in mesenteric venules of rats pretreated with selective iNOS inhibitors, 1400W or l-N6-(1-iminoethyl)-lysine. NO was localized by fluorescence microscopy, using DAF-FM. iNOS, HIF-1α and CD36 were localized by immunohistochemistr…

PharmacologyAspirinmedicine.medical_specialtybiologyChemistryCD36InflammationNitric oxideNitric oxide synthasechemistry.chemical_compoundEndocrinologyHypoxia-inducible factorsInternal medicinemedicinebiology.proteinmedicine.symptomImmunostainingIntravital microscopymedicine.drugBritish Journal of Pharmacology
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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
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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
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Pulsed Electric Fields Alter Expression of NF-κB Promoter-Controlled Gene

2021

The possibility to artificially adjust and fine‐tune gene expression is one of the key mile-stones in bioengineering, synthetic biology, and advanced medicine. Since the effects of proteins or other transgene products depend on the dosage, controlled gene expression is required for any ap-plications, where even slight fluctuations of the transgene product impact its function or other critical cell parameters. In this context, physical techniques demonstrate optimistic perspectives, and pulsed electric field technology is a potential candidate for a noninvasive, biophysical gene regulator, exploiting an easily adjustable pulse generating device. We exposed mammalian cells, transfected with a…

QH301-705.5Microsecond pulsed electric fieldSecreted alkaline phosphataseReporter assaymicrosecond pulsed electric field; inducible gene transcription control; reporter assay; secreted alkaline phosphatase; mammalian cells; cell line; NF-κBTransfectionCatalysisArticleNF-κBInorganic Chemistry03 medical and health sciencesMice0302 clinical medicineElectricityinducible gene transcription controlAnimalsHumansmammalian cellsBiology (General)Physical and Theoretical ChemistryInducible gene transcription controlQD1-999Molecular BiologySpectroscopy030304 developmental biology0303 health sciencessecreted alkaline phosphataseOrganic ChemistryNF‐κBreporter assayNF-kappa BMammalian cells:NATURAL SCIENCES::Physics [Research Subject Categories]General Medicinecell linemicrosecond pulsed electric field3. Good healthComputer Science ApplicationsChemistryGene Expression Regulation030220 oncology & carcinogenesismicrosecond pulsed electric field ; inducible gene transcription control ; reporter assay ; secreted alkaline phosphatase ; mammalian cells ; cell line ; NF-κBCell lineInternational Journal of Molecular Sciences
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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
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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
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Generation of T Follicular Helper Cells Is Mediated by Interleukin-21 but Independent of T Helper 1, 2, or 17 Cell Lineages

2008

After activation, CD4(+) helper T (Th) cells differentiate into distinct effector subsets. Although chemokine (C-X-C motif) receptor 5-expressing T follicular helper (Tfh) cells are important in humoral immunity, their developmental regulation is unclear. Here we show that Tfh cells had a distinct gene expression profile and developed in vivo independently of the Th1 or Th2 cell lineages. Tfh cell generation was regulated by ICOS ligand (ICOSL) expressed on B cells and was dependent on interleukin-21 (IL-21), IL-6, and signal transducer and activator of transcription 3 (STAT3). However, unlike Th17 cells, differentiation of Tfh cells did not require transforming growth factor beta (TGF-beta…

STAT3 Transcription FactorAdoptive cell transferCellular differentiationCellImmunologyGene ExpressionLymphocyte ActivationCXCR5ArticleInducible T-Cell Co-Stimulator LigandMiceInterleukin 21T-Lymphocyte SubsetsTransforming Growth Factor betaFollicular phasemedicineAnimalsCytotoxic T cellImmunology and AllergyCell LineageMOLIMMUNOOligonucleotide Array Sequence AnalysisB-LymphocytesT follicular helper cell differentiationbiologyInterleukin-6Reverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingInterleukinsInterleukin-17ProteinsGerminal centerCell DifferentiationT-Lymphocytes Helper-InducerTransforming growth factor betaFlow CytometryGerminal CenterAdoptive TransferImmunohistochemistryMolecular biologyMice Mutant Strainsmedicine.anatomical_structureInfectious DiseasesT helper 1CELLIMMUNOImmunologybiology.proteinInterleukin 17Signal TransductionImmunity
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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
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