Search results for "Blot"

showing 10 items of 1169 documents

DNA demethylation caused By 5-Aza-2'-Deoxycytidine induces mitotic alterations and aneuploidy

2016

Aneuploidy, the unbalanced number of chromosomes in a cell, is considered a prevalent form of genetic instability and is largely acknowledged as a condition implicated in tumorigenesis. Epigenetic alterations like DNA hypomethylation have been correlated with cancer initiation/progression. Furthermore, a growing body of evidence suggests the involvement of epigenome-wide disruption as a cause of global DNA hypomethylation in aneuploidy generation. Here, we report that the DNA hypomethylating drug 5-aza-2′-deoxycytidine (DAC), affects the correct ploidy of nearly diploid HCT-116 human cells by altering the methylation pattern of the chromosomes. Specifically, we show that a DAC-induced reduc…

0301 basic medicineAntimetabolites Antineoplastic5-aza-2'-deoxycytidine (DAC); Aneuploidy; Chromosome methylation pattern; Chromosome Section; DNA demethylation; OncologyBlotting WesternAneuploidyMitosisApoptosisBiologymedicine.disease_causeDecitabineReal-Time Polymerase Chain ReactionChromosome Section03 medical and health scienceschromosome methylation patternChromosome instabilitymedicineTumor Cells CulturedHumansEpigeneticsaneuploidyRNA Messenger5-aza-2′-deoxycytidine (DAC)Cell ProliferationGeneticsChromosome AberrationsPloidiesReverse Transcriptase Polymerase Chain ReactionDNA Methylationmedicine.disease5-aza-2'-deoxycytidine (DAC)Gene Expression Regulation NeoplasticResearch Paper: ChromosomeSettore BIO/18 - Genetica030104 developmental biologyDNA demethylationOncologyMicroscopy FluorescenceDNA methylationColonic NeoplasmsCytogenetic AnalysisCancer researchDNA demethylationAzacitidinePloidyCarcinogenesisDNA hypomethylation
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Cytotoxic effects of zearalenone and its metabolites and antioxidant cell defense in CHO-K1 cells.

2016

Zearalenone (ZEA) and its metabolites (α-zearalenol; α-ZOL, β-zearalenol; β-ZOL) are secondary metabolites of Fusarium fungi that produce cell injury. The present study explores mycotoxin-induced cell damage and cellular protection mechanisms in CHO-K1 cells. Cytotoxicity has been determined by reactive oxygen species (ROS) production and DNA damage. ROS production was determined using the fluorescein assay and DNA strand breakage by comet assay. Intracellular protection systems were glutathione (GSH), glutathione peroxidase (GPx), catalase (CAT) and superoxide dismutase (SOD). The results demonstrated that all mycotoxins increased the ROS levels up to 5.3-fold the control levels in CHO-K1 …

0301 basic medicineAntioxidantDNA damagemedicine.medical_treatmentImmunoblottingCHO CellsToxicologyAntioxidantsSuperoxide dismutase03 medical and health scienceschemistry.chemical_compoundCricetulusCricetinaemedicineAnimalsEstrogens Non-SteroidalCell damagechemistry.chemical_classificationReactive oxygen speciesGlutathione PeroxidasebiologySuperoxide DismutaseGlutathione peroxidasefood and beveragesGeneral MedicineGlutathionemedicine.diseaseCatalaseGlutathioneComet assay030104 developmental biologychemistryBiochemistrybiology.proteinZearalenoneZeranolComet AssayReactive Oxygen SpeciesOxidation-ReductionFood ScienceDNA DamageFood and chemical toxicology : an international journal published for the British Industrial Biological Research Association
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AMG900 as novel inhibitor of the translationally controlled tumor protein

2020

Abstract Introduction Cancer is one of the leading causes of death worldwide. Classical cytotoxic chemotherapy exerts high side effects and low tumor selectivity. Translationally controlled tumor protein (TCTP) is a target for differentiation therapy, a promising, new therapeutic approach, which is expected to be more selective and less toxic than cytotoxic chemotherapy. The aim of the present investigation was to identify novel TCTP inhibitors. Methods We performed in silico screening and molecular docking using a chemical library of more than 31,000 compounds to identify a novel inhibitor of TCTP. We tested AMG900 in vitro for binding to TCTP by microscale thermophoresis and co-immunoprec…

0301 basic medicineApoptosisCell Cycle ProteinsToxicologyResting Phase Cell CycleFlow cytometry03 medical and health sciences0302 clinical medicineCyclin D1Differentiation therapyCell Line TumorNeoplasmsTranslationally-controlled tumor proteinBiomarkers TumormedicineHumansCyclin D3medicine.diagnostic_testbiologyChemistryG1 PhaseTumor Protein Translationally-Controlled 1General MedicineMolecular Docking SimulationBlot030104 developmental biologyProtein Biosynthesis030220 oncology & carcinogenesisCancer cellMCF-7 CellsCancer researchbiology.proteinPhthalazinesCyclin-dependent kinase 6Chemico-Biological Interactions
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Total coumarins of Hedyotis diffusa induces apoptosis of myelodysplastic syndrome SKM-1 cells by activation of caspases and inhibition of PI3K/Akt pa…

2016

Abstract Ethnopharmacological relevance Hedyotis diffusa is an ethno-medicine used for anti-cancer treatment in the clinic of traditional Chinese medicine (TCM). The total coumarins of Hedyotis diffusa (TCHD) was a selected extract with observed antiproliferative activity, which has not been tested in treatment of myelodysplastic syndromes (MDS) or acute myeloid leukemia (AML). Aim of the study This study aimed to evaluate the apoptosis-inducing effect of TCHD on human MDS cell line (SKM-1) and explore its action mechanism in association with caspase family and PI3K/Akt signaling pathway. Materials and methods The chemical constituents and total coumarins content of TCHD were determined by …

0301 basic medicineApoptosisPharmacologyCell LineHedyotis diffusa03 medical and health sciencesPhosphatidylinositol 3-Kinases0302 clinical medicineWestern blotCoumarinsDrug DiscoverymedicineHedyotisHumansMTT assayPI3K/AKT/mTOR pathwayCaspaseCells CulturedCell ProliferationPharmacologyHedyotismedicine.diagnostic_testbiologybusiness.industryAkt/PKB signaling pathwayMesenchymal Stem Cellsbiology.organism_classification030104 developmental biologyApoptosis030220 oncology & carcinogenesisCaspasesMyelodysplastic SyndromesImmunologybiology.proteinbusinessProto-Oncogene Proteins c-aktJournal of ethnopharmacology
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Temporal quantitative phosphoproteomics of ADP stimulation reveals novel central nodes in platelet activation and inhibition

2017

Adenosine diphosphate (ADP) enhances platelet activation by virtually any other stimulant to complete aggregation. It binds specifically to the G-protein-coupled membrane receptors P2Y1 and P2Y12, stimulating intracellular signaling cascades, leading to integrin aIIbb3 activation, a process antagonized by endothelial prostacyclin. P2Y12 inhibitors are among the most successful antiplatelet drugs, however, show remarkable variability in efficacy. We reasoned whether a more detailed molecular understanding of ADP-induced protein phosphorylation could identify (1) critical hubs in platelet signaling toward aggregation and (2) novel molecular targets for antiplatelet treatment strategies. We ap…

0301 basic medicineBlood PlateletsPHOSPHATASEImmunologyBlotting WesternUBIQUITINATIONBINDING PROTEIN STXBP5Biochemistry03 medical and health scienceschemistry.chemical_compoundGTP-binding protein regulatorsP2Y12HumansProtein phosphorylationPlatelet activationIloprostPHOSPHORYLATIONCOMBINATIONChemistryPhosphoproteomicsPATHWAYSCell BiologyHematologyPlatelet ActivationSIGNALING REVEALSCell biologyAdenosine DiphosphateAdenosine diphosphate030104 developmental biologyCLOPIDOGRELPhosphorylationPROTEOMICSSECRETIONSignal transductionPlatelet Aggregation InhibitorsSignal TransductionBlood
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Circulating exosomes deliver free fatty acids from the bloodstream to cardiac cells: Possible role of CD36

2019

Regulation of circulating free fatty acid (FFA) levels and delivery is crucial to maintain tissue homeostasis. Exosomes are nanomembranous vesicles that are released from diverse cell types and mediate intercellular communication by delivering bioactive molecules. Here, we sought to investigate the uptake of FFAs by circulating exosomes, the delivery of FFA-loaded exosomes to cardiac cells and the possible role of the FFA transporter CD36 in these processes. Circulating exosomes were purified from the serum of healthy donors after an overnight fast (F) or 20 minutes after a high caloric breakfast (postprandial, PP). Western blotting, Immunogold Electron Microscopy and FACS analysis of circu…

0301 basic medicineCD36 AntigensMaleLuminescenceCD36Mice SCIDFatty Acids NonesterifiedExosomesBiochemistryFatsMiceSpectrum Analysis TechniquesAnimal CellsMice Inbred NODMedicine and Health SciencesMyocytes CardiacTissue homeostasischemistry.chemical_classificationCardiomyocytesMultidisciplinarybiologymedicine.diagnostic_testPhysicsElectromagnetic RadiationQFatty AcidsRHeartFlow CytometryLipidsCell biologyBlotSpectrophotometryPhysical SciencesMedicinelipids (amino acids peptides and proteins)FemaleCytophotometryCellular Structures and OrganellesAnatomyCellular TypesResearch ArticleAdultScienceMuscle TissueResearch and Analysis MethodsFluorescenceFlow cytometryCell Line03 medical and health sciencesIn vivomedicineDiabetes MellitusAnimalsHumansVesiclesObesityRats WistarMuscle Cells030102 biochemistry & molecular biologyFatty acidBiology and Life SciencesCell BiologyAtherosclerosisMicrovesiclesDisease Models Animal030104 developmental biologyBiological Tissuechemistrybiology.proteinCardiovascular AnatomyEx vivoPLoS ONE
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The NSL Chromatin-Modifying Complex Subunit KANSL2 Regulates Cancer Stem-like Properties in Glioblastoma That Contribute to Tumorigenesis.

2016

KANSL2 is an integral subunit of the nonspecific lethal (NSL) chromatin-modifying complex that contributes to epigenetic programs in embryonic stem cells. In this study, we report a role for KANSL2 in regulation of stemness in glioblastoma (GBM), which is characterized by heterogeneous tumor stem-like cells associated with therapy resistance and disease relapse. KANSL2 expression is upregulated in cancer cells, mainly at perivascular regions of tumors. RNAi-mediated silencing of KANSL2 in GBM cells impairs their tumorigenic capacity in mouse xenograft models. In clinical specimens, we found that expression levels of KANSL2 correlate with stemness markers in GBM stem-like cell populations. M…

0301 basic medicineCHROMATINMaleCancer ResearchCarcinogenesisCellCell SeparationMice SCIDmedicine.disease_causeMiceCANCER STEM CELLMice Inbred NODHistone AcetyltransferasesOligonucleotide Array Sequence AnalysisBrain NeoplasmsNuclear ProteinsMiddle AgedFlow CytometryImmunohistochemistryChromatinUp-Regulationmedicine.anatomical_structureOncologyGene Knockdown TechniquesNeoplastic Stem CellsHeterograftsFemaleCIENCIAS NATURALES Y EXACTASAdultKANSLOtras Ciencias BiológicasBlotting WesternGLIOBLASTOMABiologyReal-Time Polymerase Chain ReactionArticleCiencias Biológicas03 medical and health sciencesCancer stem cellmedicineBiomarkers TumorGene silencingAnimalsHumansEpigeneticsAgedEmbryonic stem cell030104 developmental biologyCancer cellImmunologyCancer researchCarcinogenesisGlioblastomaCancer research
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IL4 Primes the Dynamics of Breast Cancer Progression via DUSP4 Inhibition

2017

Abstract The tumor microenvironment supplies proinflammatory cytokines favoring a permissive milieu for cancer cell growth and invasive behavior. Here we show how breast cancer progression is facilitated by IL4 secreted by adipose tissue and estrogen receptor–positive and triple-negative breast cancer cell types. Blocking autocrine and paracrine IL4 signaling with the IL4Rα antagonist IL4DM compromised breast cancer cell proliferation, invasion, and tumor growth by downregulating MAPK pathway activity. IL4DM reduced numbers of CD44+/CD24− cancer stem-like cells and elevated expression of the dual specificity phosphatase DUSP4 by inhibiting NF-κB. Enforced expression of DUSP4 drove conversio…

0301 basic medicineCancer ResearchBlotting WesternCA 15-3Breast Neoplasms03 medical and health sciencesParacrine signalling0302 clinical medicineBreast cancerCell Line TumorTumor MicroenvironmentmedicineHumansskin and connective tissue diseasesAutocrine signallingDual-Specificity PhosphataseBlotting Western; Breast Neoplasms; Cell Line Tumor; Disease Progression; Dual-Specificity Phosphatases; Female; Flow Cytometry; Heterografts; Humans; Interleukin-4; Mitogen-Activated Protein Kinase Phosphatases; Tumor Microenvironment; Oncology; Cancer ResearchTumor microenvironmentbiologyCD44CancerFlow Cytometrymedicine.disease030104 developmental biologyOncology030220 oncology & carcinogenesisImmunologyCancer cellDisease Progressionbiology.proteinCancer researchDual-Specificity PhosphatasesHeterograftsMitogen-Activated Protein Kinase PhosphatasesFemaleInterleukin-4HeterograftMitogen-Activated Protein Kinase PhosphataseBreast NeoplasmHumanCancer Research
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Extracellular Vesicles Shed by Melanoma Cells Contain a Modified Form of H1.0 Linker Histone and H1.0 mRNA-binding Proteins

2016

Extracellular vesicles (EVs) are shed in the extracellular environment by both prokaryotes and eukaryotes. Although produced from both normal and cancer cells, malignant cells release a much higher amount of EVs, which also contain tumor-specific proteins and RNAs. We previously found that G26/24 oligodendroglioma cells shed EVs that contain the pro-apoptotic factors FasL and TRAIL1-2. Interestingly, G26/24 release, via EVs, extracellular matrix remodelling proteases3, and H1° histone protein4, and mRNA. To shed further light on the role of EVs in discarding proteins and mRNAs otherwise able to counteract proliferative signals, we studied a melanoma cell line (A375). We found that also thes…

0301 basic medicineCancer ResearchCellular differentiationBlotting WesternFluorescent Antibody TechniqueMYEF2ApoptosisRNA-binding proteinexosomesmembrane vesiclesReal-Time Polymerase Chain ReactionChromatography AffinityHistones03 medical and health sciencesH1.0 linker histone; RNA-binding proteins (RBPs); extracellular vesicles (EVs) membrane vesicles (MVs); exosomes; MYEF2Settore BIO/10 - BiochimicaTumor Cells CulturedHumansexosomeSecretionRNA MessengerSettore BIO/06 - Anatomia Comparata E Citologiamelanoma cell line (A375) myelin expression factor-2 (MYEF2)MelanomaTranscription factorCell ProliferationH1.0 linker histonebiologyReverse Transcriptase Polymerase Chain ReactionEXTRACELLULAR VESICLESRNA-Binding ProteinsRNACell DifferentiationArticlesCell biologyBlotCell Transformation Neoplastic030104 developmental biologyHistoneOncologySpectrometry Mass Matrix-Assisted Laser Desorption-IonizationCancer cellbiology.proteinRNA-binding proteins (RBPs)extracellular vesicles (EVs) membrane vesicles (MVs)
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The PDGFRβ/ERK1/2 pathway regulates CDCP1 expression in triple-negative breast cancer

2018

Background CDCP1, a transmembrane protein with tumor pro-metastatic activity, was recently identified as a prognostic marker in TNBC, the most aggressive breast cancer subtype still lacking an effective molecular targeted therapy. The mechanisms driving CDCP1 over-expression are not fully understood, although several stimuli derived from tumor microenvironment, such as factors present in Wound Healing Fluids (WHFs), reportedly increase CDCP1 levels. Methods The expression of CDCP1, PDGFRβ and ERK1/2cell was tested by Western blot after stimulation of MDA-MB-231 cells with PDGF-BB and, similarly, in presence or not of ERK1/2 inhibitor in a panel of TNBC cell lines. Knock-down of PDGFRβ was e…

0301 basic medicineCancer ResearchMAP Kinase Signaling SystemCDCP1medicine.medical_treatmentPDGFRβPDGF-BBBecaplerminTriple Negative Breast NeoplasmsBiologylcsh:RC254-282Targeted therapyReceptor Platelet-Derived Growth Factor beta03 medical and health sciences0302 clinical medicineFISHDownregulation and upregulationWestern blotAntigens CDAntigens NeoplasmCell Line TumorGeneticsmedicineHumansRNA Small InterferingReceptorTriple-negative breast cancerMitogen-Activated Protein Kinase 1Tumor microenvironmentMitogen-Activated Protein Kinase 3ERK1/2medicine.diagnostic_testMiddle Agedlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensNeoplasm ProteinsUp-RegulationGene Expression Regulation Neoplastic030104 developmental biologyOncologyGene Knockdown Techniques030220 oncology & carcinogenesisCDCP1Cancer researchImmunohistochemistryFemaleCell Adhesion MoleculesTNBCResearch ArticleIHCBMC Cancer
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