Search results for " DOM"

showing 10 items of 2750 documents

Parthenolide generates reactive oxygen species and autophagy in MDA-MB231 cells. A soluble parthenolide analogue inhibits tumour growth and metastasi…

2013

Triple-negative breast cancers (TNBCs) are clinically aggressive forms associated with a poor prognosis. We evaluated the cytotoxic effect exerted on triple-negative MDA-MB231 breast cancer cells both by parthenolide and its soluble analogue dimethylamino parthenolide (DMAPT) and explored the underlying molecular mechanism. The drugs induced a dose- and time-dependent decrement in cell viability, which was not prevented by the caspase inhibitor z-VAD-fmk. In particular in the first hours of treatment (1–3 h), parthenolide and DMAPT strongly stimulated reactive oxygen species (ROS) generation. The drugs induced production of superoxide anion by activating NADPH oxidase. ROS generation caused…

Cancer ResearchautophagyCell SurvivalparthenolideFas-Associated Death Domain ProteinImmunologyCASP8 and FADD-Like Apoptosis Regulating ProteinBreast Neoplasmsparthenolide; ROS; NOX; autophagy; breast cancer xenograft.MiceCellular and Molecular Neurosciencechemistry.chemical_compoundDownregulation and upregulationCell Line TumorSettore BIO/10 - BiochimicaAnimalsHumansParthenolidePropidium iodidebreast cancer xenograftMembrane Potential Mitochondrialchemistry.chemical_classificationReactive oxygen speciesNADPH oxidasebiologybreast cancer xenograft.SuperoxideNF-kappa BRNA-Binding ProteinsROSCell BiologyNOXXenograft Model Antitumor AssaysMolecular biologyNuclear Pore Complex ProteinsVascular endothelial growth factorchemistryCell cultureCancer researchbiology.proteinCalciumFemaleOriginal ArticleReactive Oxygen SpeciesSesquiterpenes
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Comprehensive Analysis of VEGFR2 Expression in HPV-Positive and -Negative OPSCC Reveals Differing VEGFR2 Expression Patterns

2021

VEGF signaling regulated by the vascular endothelial growth factor receptor 2 (VEGFR2) plays a decisive role in tumor angiogenesis, initiation and progression in several tumors including HNSCC. However, the impact of HPV-status on the expression of VEGFR2 in OPSCC has not yet been investigated, although HPV oncoproteins E6 and E7 induce VEGF-expression. In a series of 56 OPSCC with known HPV-status, VEGFR2 expression patterns were analyzed both in blood vessels from tumor-free and tumor-containing regions and within tumor cells by immunohistochemistry using densitometry. Differences in subcellular colocalization of VEGFR2 with endothelial, tumor and stem cell markers were determined by doub…

Cancer Researchcancer stem cellAngiogenesisNeoplasms. Tumors. Oncology. Including cancer and carcinogensKinase insert domain receptorBiologyrespiratory systemStem cell markerArticlemedicine.anatomical_structureOncologyCancer stem cellvascular endothelial growth factor receptor 2Cancer cellCancer researchmedicinecardiovascular systemoropharyngeal squamous cell carcinomaImmunohistochemistryAutocrine signallinghuman papillomavirusRC254-282Blood vesselcirculatory and respiratory physiology
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Mammary-derived growth inhibitor (MDGI) interacts with integrin α-subunits and suppresses integrin activity and invasion

2010

The majority of mortality associated with cancer is due to formation of metastases from the primary tumor. Adhesion mediated by different integrin heterodimers has an important role during cell migration and invasion. Protein interactions with the β1-integrin cytoplasmic tail are known to influence integrin affinity for extracellular ligands, but regulating binding partners for the α-subunit cytoplasmic tails have remained elusive. In this study, we show that mammary-derived growth inhibitor (MDGI) (also known as FABP-3 or H-FABP) binds directly to the cytoplasmic tail of integrin α-subunits and its expression inhibits integrin activity. In breast cancer cell lines, MDGI expression correlat…

Cancer Researchmedicine.disease_causemigrationCD49cCollagen receptor0302 clinical medicineCell Movement0303 health sciencesCell migrationMiddle Agedinvasion3. Good healthCell biologyExtracellular MatrixadhesionIntegrin alpha MMDGI030220 oncology & carcinogenesis/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_beingIntegrin beta 6FemaleFatty Acid Binding Protein 3Integrin alpha Chainsmedicine.medical_specialtyintegrinIntegrinMolecular Sequence DataBreast NeoplasmsBiologyFatty Acid-Binding ProteinsCollagen Type IDisease-Free Survival03 medical and health sciencesbreast cancerSDG 3 - Good Health and Well-beingInternal medicineCell Line TumorGeneticsmedicineHumansNeoplasm InvasivenessProtein Interaction Domains and MotifsAmino Acid SequenceMolecular Biology030304 developmental biologyFibronectinsFibronectinEndocrinologybiology.proteinCarcinogenesisOncogene
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Intratumoral Heterogeneity in EGFR-Mutant NSCLC Results in Divergent Resistance Mechanisms in Response to EGFR Tyrosine Kinase Inhibition

2015

Abstract Non–small cell lung cancers (NSCLC) that have developed resistance to EGF receptor (EGFR) tyrosine kinase inhibitor (TKI), including gefitinib and erlotinib, are clinically linked to an epithelial-to-mesenchymal transition (EMT) phenotype. Here, we examined whether modulating EMT maintains the responsiveness of EGFR-mutated NSCLCs to EGFR TKI therapy. Using human NSCLC cell lines harboring mutated EGFR and a transgenic mouse model of lung cancer driven by mutant EGFR (EGFR-Del19-T790M), we demonstrate that EGFR inhibition induces TGFβ secretion followed by SMAD pathway activation, an event that promotes EMT. Chronic exposure of EGFR-mutated NSCLC cells to TGFβ was sufficient to ind…

Cancer Researchmedicine.drug_classCellBiologymedicine.diseaseArticleTyrosine-kinase inhibitorrespiratory tract diseasesmedicine.anatomical_structureGefitinibOncologyProtein kinase domainImmunologymedicineCancer researchEpithelial–mesenchymal transitionErlotinibSignal transductionLung cancerneoplasmsmedicine.drugCancer Research
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Hypoxia-induced epithelial VEGF-C/VEGFR-3 upregulation in carcinoma cell lines

2008

Adaptation to hypoxia, a universal hallmark of carcinomas, is a critical step for tumor cell survival and growth. One of the principal regulators of hypoxia-responsive pathways is the transcription factor hypoxia-inducible factor-1 alpha (HIF-1 alpha). Currently, it is known that tumoral production of members of the vascular endothelial growth factor (VEGF)-family (VEGFs) may promote tumor growth and progression by acting on carcinoma cells that express the cognate receptors (VEGFRs). However, the influence of hypoxia in the formation of such a tumoral VEGF/VEGFR loop is not completely understood. In the present study we examined the potential existence of a HIF-1 alpha/VEGF/VEGFR autocrine…

Cancer Researchmedicine.medical_specialtyLung NeoplasmsVascular Endothelial Growth Factor CCellBreast NeoplasmsBiologychemistry.chemical_compoundDownregulation and upregulationCell Line TumorInternal medicinemedicineHumansAutocrine signallingVascular Endothelial Growth Factor Receptor-1CarcinomaKinase insert domain receptorCell cycleHypoxia-Inducible Factor 1 alpha SubunitVascular Endothelial Growth Factor Receptor-3Vascular Endothelial Growth Factor Receptor-2Cell HypoxiaUp-RegulationGene Expression Regulation NeoplasticVascular endothelial growth factorAutocrine CommunicationHIF1AEndocrinologymedicine.anatomical_structureOncologyVascular endothelial growth factor CchemistryCancer researchColorectal NeoplasmsInternational Journal of Oncology
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Cyclooxygenase-2 inhibition induces apoptosis signaling via death receptors and mitochondria in hepatocellular carcinoma.

2006

AbstractInhibition of cyclooxygenase (COX)-2 elicits chemopreventive and therapeutic effects in solid tumors that are coupled with the induction of apoptosis in tumor cells. We investigated the mechanisms by which COX-2 inhibition induces apoptosis in hepatocellular carcinoma (HCC) cells. COX-2 inhibition triggered expression of the CD95, tumor necrosis factor (TNF)-R, and TNF-related apoptosis-inducing ligand (TRAIL)-R1 and TRAIL-R2 death receptors. Addition of the respective specific ligands further increased apoptosis, indicating that COX-2 inhibition induced the expression of functional death receptors. Overexpression of a dominant-negative Fas-associated death domain mutant reduced COX…

Cancer Researchmedicine.medical_specialtyProgrammed cell deathCarcinoma HepatocellularApoptosisMitochondria LiverBiologyTransfectionReceptors Tumor Necrosis FactorInternal medicineCell Line TumormedicineHumansfas ReceptorDeath domainInhibitor of apoptosis domainSulfonamidesCyclooxygenase 2 InhibitorsIntrinsic apoptosisLiver NeoplasmsFas receptorReceptors TNF-Related Apoptosis-Inducing LigandEndocrinologyOncologyUVB-induced apoptosisApoptosisCelecoxibCyclooxygenase 2Cancer researchPyrazolesSignal transductionSignal TransductionCancer research
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Abstract 753: Genomic alterations of autophagy genes disrupts autophagic flux in human lung adenocarcinomas

2015

Abstract Targeted therapy using EGFR tyrosine kinase inhibitor (TKI) is a standard therapy for a subset of non-small cell lung cancer (NSCLC) patients with lung adenocarcinomas (LADs) harboring EGFR kinase domain mutations; however, EGFR TKI therapy shows limited efficacy due to de novo and acquired resistance. Consequently, formulating strategies to potentiate the efficacy of EGFR TKI is of great interest. In EGFR TKI sensitive cells harboring EGFR mutation, it has been shown that EGFR inhibition induces autophagy to protect the cells from metabolic stress. Hydroxychloroquine (HQ), an inhibitor of autophagy, has been shown to potentiate EGFR TKIs in preclinical models, however, preliminary…

Cancer Researchmedicine.medical_treatmentATG5AutophagyBiologyBioinformaticsmedicine.diseaseTargeted therapyOncologyProtein kinase domainChromosome 3Cancer researchmedicineErlotinibLung cancerGenemedicine.drugCancer Research
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Validating an apple dry matter production model with whole canopy gas exchange measurements in the field

1999

The simplified apple dry matter production model developed by Lakso and Johnson (1990) was modified by inputing tree-specific parameters from a study of seasonal growth and gas exchange of 4-year-old Empire/M.9 apple trees, and light and temperature response curves developed for Empire apple organs. Measurements of the seasonal trend of diurnal net C02 and canopy water vapor exchange were made at intervals on three four-year-old 'Empire'/M.9 slender spindle apple trees in the orchard from 10 days after bloom until 25 days after harvest. The tree canopies were enclosed in clear plastic "balloon- type" chambers (similar to Corelli and Magnanini, 1993) that was monitored continuously for more …

CanopyAgronomyField (physics)Production modelLight Malus domestica Borkh Photosynthesis Respiration Seasonal gas exchange TemperatureEnvironmental scienceDry matterHorticulture
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Effects of partial rootzone drying and rootstock vigour on dry matter partitioning of apple trees (Malus domesticacvar Pink Lady)

2011

SUMMARYThe effects of partial rootzone drying (PRD) and rootstock vigour on dry matter accumulation and partitioning among leaves, shoots, fruits, frame and roots of apple trees (Malus domesticaBorkh. cvar Pink Lady) were investigated in 2005 near Caltavuturo, in Sicily. In a first field trial, trees on MM.106 rootstock were subjected to: conventional irrigation (CI), maintaining soil moisture above 0·80 of field capacity; PRD irrigation, where alternating sides of the rootzone received 0·50 of the CI irrigation water; and continuous deficit irrigation (DI), where 0·50 of the CI water was equally applied to both sides of the rootzone. In a second trial, trees on M.9 or MM.106 were subjected…

CanopyMalus domestica deficit irrigation carbon allocation root growth.IrrigationMalusVegetative reproductionDeficit irrigationBiologybiology.organism_classificationSettore AGR/03 - Arboricoltura Generale E Coltivazioni ArboreeHorticultureBotanyShootGeneticsAnimal Science and ZoologyDry matterRootstockAgronomy and Crop ScienceThe Journal of Agricultural Science
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Down-regulation of OPA1 alters mouse mitochondrial morphology, PTP function, and cardiac adaptation to pressure overload

2012

AIMS: The optic atrophy 1 (OPA1) protein is an essential protein involved in the fusion of the mitochondrial inner membrane. Despite its high level of expression, the role of OPA1 in the heart is largely unknown. We investigated the role of this protein in Opa1(+/-) mice, having a 50% reduction in OPA1 protein expression in cardiac tissue. METHODS AND RESULTS: In mutant mice, cardiac function assessed by echocardiography was not significantly different from that of the Opa1(+/+). Electron and fluorescence microscopy revealed altered morphology of the Opa1(+/-) mice mitochondrial network; unexpectedly, mitochondria were larger with the presence of clusters of fused mitochondria and altered c…

Cardiac function curveendocrine systemPhysiologyAdaptation BiologicalDown-RegulationBiologyMitochondrionMitochondrial Membrane Transport ProteinsPermeabilityGTP PhosphohydrolasesMitochondrial ProteinsMice03 medical and health sciencesMitochondrial membrane transport protein0302 clinical medicinePhysiology (medical)Optic Atrophy Autosomal DominantPressuremedicineAnimalsMyocyteMyocytes CardiacInner mitochondrial membrane030304 developmental biologyMice KnockoutPressure overload0303 health sciencesMitochondrial Permeability Transition Poremedicine.diseaseeye diseasesMitochondriaCell biologyBiochemistryMitochondrial permeability transition poreMitochondrial Membranesbiology.proteinOptic Atrophy 1Cardiology and Cardiovascular Medicine030217 neurology & neurosurgeryCardiovascular Research
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