Search results for "Research Paper"

showing 10 items of 477 documents

Severe metabolic alterations in liver cancer lead to ERK pathway activation and drug resistance

2020

Background: The extracellular signal-regulated kinase (ERK) pathway regulates cell growth, and is hyper-activated and associated with drug resistance in hepatocellular carcinoma (HCC). Metabolic pathways are profoundly dysregulated in HCC. Whether an altered metabolic state is linked to activated ERK pathway and drug response in HCC is unaddressed. Methods: We deprived HCC cells of glutamine to induce metabolic alterations and performed various assays, including metabolomics (with 13C-glucose isotope tracing), microarray analysis, and cell proliferation assays. Glutamine-deprived cells were also treated with kinase inhibitors (e.g. Sorafenib, Erlotinib, U0126 amongst other MEK inhibitors). …

Life sciences; biology0301 basic medicineSorafenibMAPK/ERK pathwayCarcinoma HepatocellularResearch paperMAP Kinase Signaling SystemGlutamineProliferationlcsh:MedicineAntineoplastic AgentsGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciences0302 clinical medicineDownregulation and upregulationddc:570medicineSerineHumansHCCProtein Kinase InhibitorsCell Proliferationlcsh:R5-920Cell growthChemistryKinaseMicroarray analysis techniquesLiver Neoplasmslcsh:RGeneral MedicineHep G2 Cellsdigestive system diseasesMetabolic pathway030104 developmental biologyAnaerobic glycolysisDrug Resistance NeoplasmKinase inhibitors030220 oncology & carcinogenesisCancer researchMetabolomeMetabolic stateAerobic glycolysisTranscriptomelcsh:Medicine (General)medicine.drugEBioMedicine
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Association between the rs6950982 polymorphism near the SERPINE1 gene and blood pressure and lipid parameters in a high-cardiovascular-risk populatio…

2012

The SERPINE1 (serpin peptidase inhibitor, clade E, member 1) gene, better known by its previous symbol PAI-1 (plasminogen activator inhibitor 1), has been associated with cardiovascular phenotypes with differing results. Our aim was to examine the association between the rs6950982 (G  A) near the SERPINE1 gene, blood pressure (BP) and plasma lipid concentrations as well as the modulation of the polymorphism effects by adherence to Mediterranean diet (AMD). We studied 945 high-cardiovascular-risk subjects. Biochemical, clinical, dietary and genetic data (rs6950982) were obtained. We also determined the common rs1799768 (4G/5G), for checking independent effects. AMD was measured by a validate…

Linkage disequilibriummedicine.medical_specialtyMediterranean dietEndocrinology Diabetes and MetabolismPopulationBiologyCardiovascularchemistry.chemical_compoundPolymorphism (computer science)Internal medicineMediterranean dietmedicineGeneticsAlleleeducationNutrigeneticsGeneticseducation.field_of_studyTriglycerideLipidsBlood pressureEndocrinologychemistryPlasminogen activator inhibitor-1Blood pressureResearch Paper
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Pro-oxidant activity of indicaxanthin from Opuntia ficus indica modulates arachidonate metabolism and prostaglandin synthesis through lipid peroxide …

2014

Macrophages come across active prostaglandin (PG) metabolism during inflammation, shunting early production of pro-inflammatory towards anti-inflammatory mediators terminating the process. This work for the first time provides evidence that a phytochemical may modulate the arachidonate (AA) metabolism in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages, promoting the ultimate formation of anti-inflammatory cyclopentenone 15deoxy-PGJ2. Added 1 h before LPS, indicaxanthin from Opuntia Ficus Indica prevented activation of nuclear factor-κB (NF-κB) and over-expression of PGE2 synthase-1 (mPGES-1), but up-regulated cyclo-oxygenase-2 (COX-2) and PGD2 synthase (H-PGDS), with final product…

LipopolysaccharidesLipid PeroxidesLipopolysaccharidePyridinesPhytochemicalsClinical BiochemistryProstaglandinIndicaxanthinmedicine.disease_causeBiochemistryCell LineMiceStructure-Activity Relationshipchemistry.chemical_compoundmedicineAnimalslcsh:QH301-705.5Inflammationlcsh:R5-920Arachidonic AcidNADPH oxidaseDose-Response Relationship DrugLipid peroxidebiologyMacrophagesOrganic ChemistryOpuntiaMetabolismOxidantsPro-oxidantBetaxanthinslcsh:Biology (General)chemistryBiochemistryOxidative stressFruitIndicaxanthin Phytochemicals Eicosanoids Inflammation Oxidative stress.Prostaglandinsbiology.proteinEicosanoidslipids (amino acids peptides and proteins)lcsh:Medicine (General)IndicaxanthinOxidative stressResearch PaperRedox Biology
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Bcl-2 is a negative regulator of interleukin-1β secretion in murine macrophages in pharmacological-induced apoptosis

2010

BACKGROUND AND PURPOSE Cucurbitacin R, a natural anti-inflammatory product, has been shown to exhibit activity against both adjuvant-induced arthritis and delayed-type hypersensitivity reactions induced by various agents. Previous studies have demonstrated that the effects of cucurbitacin R stem from its inhibition of both cytokine production and lymphocyte proliferation. EXPERIMENTAL APPROACHES Effects of cucurbitacin R were investigated on lipopolysaccharide-stimulated RAW 264.7 cells. Cell cycle evolution was analysed by flow cytometry, detection of apoptosis by DNA ladder, Bcl-2, p21, p53, Bax, cleaved caspase-1 (p10), caspase-9, and caspase-3, cleaved caspase (p17) and interleukin-1β d…

LipopolysaccharidesProgrammed cell deathinterleukin-1βmedicine.medical_treatmentBlotting WesternInterleukin-1betaCaspase 1caspase-1Caspase 3Lymphocyte proliferationBiologyTransfectionCell LineMiceRAW 264.7 macrophagesmedicineAnimalsBcl-2RNA Small InterferingPharmacologyMembrane Potential MitochondrialCaspase 3Reverse Transcriptase Polymerase Chain ReactionMacrophagesAnti-Inflammatory Agents Non-SteroidalCaspase 1Cell CycleapoptosisCell cycleFlow CytometryMolecular biologyResearch PapersTriterpenescucurbitacin RCytokineProto-Oncogene Proteins c-bcl-2Cell cultureApoptosis
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Quaking and miR-155 interactions in inflammation and leukemogenesis.

2015

Quaking (QKI) is a tumor-suppressor gene encoding a conserved RNA-binding protein, whose expression is downregulated in several solid tumors. Here we report that QKI plays an important role in the immune response and suppression of leukemogenesis. We show that the expression of Qki is reduced in lipopolysaccharide (LPS)-challenged macrophages, suggesting that Qki is a key regulator of LPS signaling pathway. Furthermore, LPS-induced downregulation of Qki expression is miR-155-dependent. Qki overexpression impairs LPS-induced phosphorylation of JNK and particularly p38 MAPKs, in addition to increasing the production of anti-inflammatory cytokine IL-10. In contrast, Qki ablation decreases Fas …

LipopolysaccharidesTime Factorsmedicine.medical_treatmentmedicine.disease_causeTransgenicMiceInnatePhosphorylationChronicB-LymphocytesLeukemiaRNA-Binding ProteinsU937 CellsLymphocyticCell biologyCytokineOncologyPhosphorylationCytokinesCLL; Glioblastoma; Inflammation; MiR-155; QKI; Animals; Apoptosis Regulatory Proteins; B-Lymphocytes; Case-Control Studies; Cytokines; Humans; Immunity Innate; Inflammation; Leukemia Lymphocytic Chronic B-Cell; Lipopolysaccharides; Macrophages; Mice; Mice Transgenic; MicroRNAs; Mitogen-Activated Protein Kinases; Phosphorylation; RAW 264.7 Cells; RNA-Binding Proteins; Signal Transduction; Time Factors; Transfection; U937 Cells; OncologySignal transductionMitogen-Activated Protein KinasesSignal Transductionp38 mitogen-activated protein kinasesOncology and CarcinogenesisMice TransgenicTransfectionNOmiR-155miR-155Downregulation and upregulationmicroRNAmedicineAnimalsHumansInflammationQKIbusiness.industryMacrophagesB-CellImmunityglioblastomaLeukemia Lymphocytic Chronic B-CellImmunity InnateMicroRNAsRAW 264.7 CellsCase-Control StudiesImmunologyCarcinogenesisbusinessApoptosis Regulatory ProteinsCLLPriority Research Paper
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GDF11 induces mild hepatic fibrosis independent of metabolic health

2020

BACKGROUND & AIMS: Growth Differentiation Factor 11 (GDF11) is an anti-aging factor, yet its role in liver diseases is not established. We evaluated the role of GDF11 in healthy conditions and in the transition from non-alcoholic fatty liver disease (NAFLD) to non-alcoholic steatohepatitis (NASH). RESULTS: GDF11 mRNA levels positively correlated with NAFLD activity score and with CPT1, SREBP, PPAR? and Col1A1 mRNA levels, and associated to portal fibrosis, in morbidly obese patients with NAFLD/NASH. GDF11-treated mice showed mildly exacerbated hepatic collagen deposition, accompanied by weight loss and without changes in liver steatosis or inflammation. GDF11 triggered ALK5-dependent SMAD2/…

Liver CirrhosisMaleAgingSettore MED/09 - Medicina Interna*liverLiver Cirrhosis ExperimentalFetgeWeight lossFibrosisfibrosis; growth differentiation factor 11; liver; NAFLD; NASHNon-alcoholic Fatty Liver DiseaseGrowth differentiation factor 11Fatty liverNASH*fibrosisMiddle AgedObesity MorbidGrowth Differentiation FactorsLiverBone Morphogenetic ProteinsDisease ProgressionFemalemedicine.symptomResearch PaperSignal TransductionAdultmedicine.medical_specialtygrowth differentiation factor 11Inflammationliverdigestive systemCell LineEnvellimentInternal medicineNAFLDmedicineHepatic Stellate CellsAnimalsHumansddc:612*growth differentiation factor 11business.industry*NAFLDfibrosisnutritional and metabolic diseasesCell Biologyliver NAFLD NASH fibrosis growth differentiation factor 11*NASHmedicine.diseaseFibrosisdigestive system diseasesMice Inbred C57BLEndocrinologyPortal fibrosisCase-Control StudiesGDF11Hepatic stellate cellSteatohepatitisHepatic fibrosisbusiness
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Inhibition of c-MYC with involvement of ERK/JNK/MAPK and AKT pathways as a novel mechanism for shikonin and its derivatives in killing leukemia cells

2015

Leukemia remains life-threatening despite remarkable advances in chemotherapy. The poor prognosis and drug resistance are challenging treatment. Novel drugs are urgently needed. Shikonin, a natural naphthoquinone, has been previously shown by us to be particularly effective towards various leukemia cell lines compared to solid tumors. However, the underlying mechanisms are still poorly understood. Here, we investigated shikonin and 14 derivatives on U937 leukemia cells. Four derivatives (isobutyrylshikonin, 2-methylbutyrylshikonin, isovalerylshikonin and β,β-dimethylacrylshikonin) were more active than shikonin. AnnexinV-PI analysis revealed that shikonins induced apoptosis. Cell cycle G1/S…

MAPK/ERK pathwayMAP Kinase Signaling Systemshikonin and its derivativesJurkat cellsProto-Oncogene Proteins c-mycCell Line TumormedicineHumansacute leukemiaExtracellular Signal-Regulated MAP KinasesProtein kinase BPI3K/AKT/mTOR pathwayMitogen-Activated Protein Kinase KinasesLeukemiaU937 cellERK/JNK/MAP kinasesbusiness.industryAnti-Inflammatory Agents Non-SteroidalJNK Mitogen-Activated Protein KinasesU937 CellsCell cyclemedicine.diseaseLeukemiac-MYCAKT pathwayOncologyCancer researchSignal transductionbusinessProto-Oncogene Proteins c-aktResearch PaperNaphthoquinonesSignal TransductionOncotarget
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Influences of TP53 and the anti-aging DDR1 receptor in controlling Raf/MEK/ERK and PI3K/Akt expression and chemotherapeutic drug sensitivity in prost…

2020

Background TP53 plays critical roles in sensitivity to chemotherapy, and aging. Collagen is very important in aging. The molecular structure and biochemical properties of collagen changes during aging. The discoidin domain receptor (DDR1) is regulated in part by collagen. Elucidating the links between TP53 and DDR1 in chemosensitivity and aging could improve therapies against cancer and aging. Results Restoration of WT-TP53 activity resulted in increased sensitivity to chemotherapeutic drugs and elevated expression of key components of the Raf/MEK/ERK, PI3K/Akt and DDR1 pathways. DDR1 could modulate the levels of Raf/MEK/ERK and PI3K/Akt pathways as well as sensitize the cells to chemothera…

MAPK/ERK pathwayMalecollagenAgingRAF/MEK/ERKMAP Kinase Signaling SystemAntineoplastic Agentsdiscoidin domain receptor (DDR1)DDRCollagen receptorPhosphatidylinositol 3-KinasesDiscoidin Domain Receptor 1Cell Line TumorHumansRapamycinTP53ReceptorProtein kinase BPI3K/AKT/mTOR pathwayDDR1ChemistryWild typeProstateProstatic NeoplasmschemoresistanceCell Biologyprostate cancerDrug Resistance NeoplasmMutationCancer researchraf KinasesTumor Suppressor Protein p53Discoidin domainResearch Paper
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The three-dimensional structure of Drosophila melanogaster (6–4) photolyase at room temperature

2021

A crystal structure of a photolyase at room temperature confirms the structural information obtained from cryogenic crystallography and paves the way for time-resolved studies of the photolyase at an X-ray free-electron laser.

MECHANISMMaterials scienceAbsorption spectroscopyDNA repairfotobiologia02 engineering and technologyCrystal structureREPAIR ACTIVITY03 medical and health sciencesCOLI DNA PHOTOLYASEX-RAY-DIFFRACTIONCryptochromeStructural BiologyAnimalsserial crystallographyCRYSTAL-STRUCTURECRYPTOCHROMEPhotolyaseSERIAL FEMTOSECOND CRYSTALLOGRAPHY030304 developmental biology0303 health sciencesCrystallographyflavoproteinsFADResolution (electron density)TemperaturebanaanikärpänenDNAkidetiede(6-4) photolyase021001 nanoscience & nanotechnologyResearch PapersRADICAL TRANSFER(6–4) photolyaseroom-temperature structureCrystallographyphotolyasesDrosophila melanogasterRECONSTITUTIONX-ray crystallography1182 Biochemistry cell and molecular biologylämpötilaproteiinit0210 nano-technologyDeoxyribodipyrimidine Photo-LyasePHOTOACTIVATIONVisible spectrumActa Crystallographica Section D Structural Biology
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Gallium modulates osteoclastic bone resorption in vitro without affecting osteoblasts.

2010

Gallium (Ga) has been shown to be effective in the treatment of disorders associated with accelerated bone loss, including cancer-related hypercalcemia and Paget's disease. These clinical applications suggest that Ga could reduce bone resorption. However, few studies have studied the effects of Ga on osteoclastic resorption. Here, we have explored the effects of Ga on bone cells in vitro.In different osteoclastic models [osteoclasts isolated from long bones of neonatal rabbits (RBC), murine RAW 264.7 cells and human CD14-positive cells], we have performed resorption activity tests, staining for tartrate resistant acid phosphatase (TRAP), real-time polymerase chain reaction analysis, viabili…

MESH: Bone ResorptionMESH: RabbitsGallium[SDV.BC.IC] Life Sciences [q-bio]/Cellular Biology/Cell Behavior [q-bio.CB]MESH: Base Sequence[SDV.BBM.BM] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyMiceMESH: Alkaline PhosphataseMESH: Reverse Transcriptase Polymerase Chain Reaction[SDV.BC.IC]Life Sciences [q-bio]/Cellular Biology/Cell Behavior [q-bio.CB]MESH: Animals[SDV.BBM.BC] Life Sciences [q-bio]/Biochemistry Molecular Biology/Biochemistry [q-bio.BM]Cells Cultured[SDV.MHEP.RSOA] Life Sciences [q-bio]/Human health and pathology/Rhumatology and musculoskeletal systemReverse Transcriptase Polymerase Chain ReactionCell DifferentiationMESH: GalliumResearch Papers[SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry Molecular Biology/Biomolecules [q-bio.BM]Isoenzymes[SDV.MHEP.RSOA]Life Sciences [q-bio]/Human health and pathology/Rhumatology and musculoskeletal systemMESH: Isoenzymes[SDV.BBM.GTP] Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN]RabbitsMESH: Cells Culturedmusculoskeletal diseasesMESH: Cell DifferentiationMESH: DNA PrimersAcid Phosphatase[SDV.CAN]Life Sciences [q-bio]/CancerIn Vitro TechniquesMESH: Acid Phosphatase[SDV.CAN] Life Sciences [q-bio]/Cancer[SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN]AnimalsHumansBone Resorption[SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry Molecular Biology/Biochemistry [q-bio.BM]MESH: Tartrate-Resistant Acid Phosphatase[SDV.IB.BIO]Life Sciences [q-bio]/Bioengineering/BiomaterialsMESH: MiceDNA PrimersMESH: In Vitro TechniquesMESH: OsteoblastsOsteoblastsMESH: HumansBase SequenceTartrate-Resistant Acid Phosphatase[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyAlkaline Phosphatase[SDV.IB.BIO] Life Sciences [q-bio]/Bioengineering/Biomaterials
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