Search results for "Assay"

showing 10 items of 2241 documents

Artesunate derived from traditional Chinese medicine induces DNA damage and repair.

2008

Abstract Artesunate is a semisynthetic derivative from artemisinin, a natural product from the Chinese herb Artemisia annua L. It exerts antimalarial activity, and, additionally, artemisinin and its derivatives are active against cancer cells. The active moiety is an endoperoxide bridge. Its cleavage leads to the formation of reactive oxygen species and carbon-centered radicals. These highly reactive molecules target several proteins in Plasmodia, which is thought to result in killing of the microorganism. DNA damage induced by artemisinins has not yet been described. Here, we show that artesunate induces apoptosis and necrosis. It also induces DNA breakage in a dose-dependent manner as sho…

Cancer ResearchKu80DNA RepairDNA repairDNA damageBlotting WesternArtesunateFluorescent Antibody TechniqueApoptosisBiologyCell Linechemistry.chemical_compoundCricetulusCricetinaeAnimalsMedicine Chinese TraditionalBase excision repairDNAMolecular biologyArtemisininsComet assayOncologychemistryArtesunateCancer cellComet AssayHomologous recombinationDNA DamageCancer research
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β-Catenin Contributes to Lung Tumor Development Induced by EGFR Mutations

2014

Abstract The discovery of somatic mutations in EGFR and development of EGFR tyrosine kinase inhibitors (TKI) have revolutionized treatment for lung cancer. However, resistance to TKIs emerges in almost all patients and currently no effective treatment is available. Here, we show that β-catenin is essential for development of EGFR-mutated lung cancers. β-Catenin was upregulated and activated in EGFR-mutated cells. Mutant EGFR preferentially bound to and tyrosine phosphorylated β-catenin, leading to an increase in β-catenin–mediated transactivation, particularly in cells harboring the gefitinib/erlotinib-resistant gatekeeper EGFR-T790M mutation. Pharmacologic inhibition of β-catenin suppresse…

Cancer ResearchLung NeoplasmsCarcinogenesisAfatinibMutation MissenseAntineoplastic AgentsMice TransgenicAfatinibmedicine.disease_causeArticleTransactivationGefitinibCarcinoma Non-Small-Cell LungCell Line TumormedicineAnimalsHumansEpidermal growth factor receptorLung cancerbeta CateninMutationbiologyProtein Stabilitymedicine.diseaseXenograft Model Antitumor AssaysTumor BurdenUp-Regulationrespiratory tract diseasesErbB ReceptorsGene Expression Regulation NeoplasticHEK293 CellsOncologyDoxycyclineCateninImmunologyQuinazolinesCancer researchbiology.proteinCarcinogenesismedicine.drugCancer Research
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Targeting transcriptional addictions in small cell lung cancer with a covalent CDK7 inhibitor.

2014

Small cell lung cancer (SCLC) is an aggressive disease with high mortality, and the identification of effective pharmacological strategies to target SCLC biology represents an urgent need. Using a high-throughput cellular screen of a diverse chemical library, we observe that SCLC is sensitive to transcription-targeting drugs, in particular to THZ1, a recently identified covalent inhibitor of cyclin-dependent kinase 7. We find that expression of super-enhancer-associated transcription factor genes, including MYC family proto-oncogenes and neuroendocrine lineage-specific factors, is highly vulnerability to THZ1 treatment. We propose that downregulation of these transcription factors contribut…

Cancer ResearchLung NeoplasmsTranscription GeneticMolecular Sequence DataAntineoplastic AgentsBiologyBioinformaticsArticleMiceSuper-enhancerDownregulation and upregulationCell Line TumorMedicineAnimalsHumansEnzyme InhibitorsneoplasmsTranscription factorRegulation of gene expressionbusiness.industryCell BiologyNeoplasms ExperimentalSequence Analysis DNASmall Cell Lung CarcinomaXenograft Model Antitumor AssayshumanitiesCyclin-Dependent Kinasesrespiratory tract diseasesHigh-Throughput Screening AssaysGene Expression Regulation NeoplasticOncologyCovalent bondCancer cellCancer researchNon small cellSmall Cell Lung CarcinomaCyclin-dependent kinase 7businessTranscription Factor GeneCDK12Transcription FactorsCancer cell
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Bispecific antibodies targeting tumor-associated antigens and neutralizing complement regulators increase the efficacy of antibody-based immunotherap…

2015

The efficacy of antibody-based immunotherapy is due to the activation of apoptosis, the engagement of antibody-dependent cellular cytotoxicity and complement-dependent cytotoxicity (CDC). We developed a novel strategy to enhance CDC using bispecific antibodies (bsAbs) that neutralize the C-regulators CD55 and CD59 to enhance C-mediated functions. Two bsAbs (MB20/55 and MB20/59) were designed to recognize CD20 on one side. The other side neutralizes CD55 or CD59. Analysis of CDC revealed that bsAbs could kill 4-25 times more cells than anti-CD20 recombinant antibody in cell lines or cells isolated from patients with chronic lymphocytic leukemia. The pharmacokinetics of the bsAbs was evaluate…

Cancer ResearchLymphomaMacrophageChronic lymphocytic leukemiamedicine.medical_treatmentAntibodieCell SeparationMice SCIDMiceAntibodies BispecificCloning MolecularCytotoxicityCD20LeukemiabiologyCD55 AntigensMedicine (all)HematologyFlow CytometryBurkitt LymphomaKiller Cells NaturalLeukemiaOncologyFemaleImmunotherapyAntibodybispecific antibodiesExperimental Lymphoma Mice MiceHumanComplement System ProteinCD59 AntigensEnzyme-Linked Immunosorbent AssayAntigens CD59Antigens CD55AntibodiesExperimentalAntigenbispecific antibodies; Leukemia; Experimental Lymphoma Mice Mice; complement systemmedicineAnimalsHumanscomplement systemAnimalMacrophagesAntibody-Dependent Cell CytotoxicityImmunotherapyComplement System Proteinsmedicine.diseaseAntigens CD20Complement systembispecific antibodieDisease Models AnimalAnesthesiology and Pain MedicineMicroscopy FluorescenceImmunologybiology.protein
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Multivalent DR5 peptides activate the TRAIL death pathway and exert tumoricidal activity.

2010

Abstract Ongoing clinical trials are exploring anticancer approaches based on signaling by TRAIL, a ligand for the cell death receptors DR4 and DR5. In this study, we report on the selective apoptotic effects of multivalent DR5 binding peptides (TRAILmim/DR5) on cancer cells in vitro and in vivo. Surface plasmon resonance revealed up to several thousand-fold increased affinities of TRAILmim/DR5-receptor complexes on generation of divalent and trivalent molecules, the latter of which was achieved with a conformationally restricted adamantane core. Notably, only multivalent molecules triggered a substantial DR5-dependent apoptotic response in vitro. In tumor models derived from human embryoni…

Cancer ResearchMembrane transport and intracellular motility [NCMLS 5]Apoptosis[CHIM.THER]Chemical Sciences/Medicinal Chemistry[ SDV.CAN ] Life Sciences [q-bio]/CancerTNF-Related Apoptosis-Inducing LigandMice0302 clinical medicineStilbenesReceptorCells Cultured0303 health sciencesDrug Synergism[ CHIM.THER ] Chemical Sciences/Medicinal ChemistryLigand (biochemistry)Tumor Burden3. Good healthMitochondrial medicine [IGMD 8]Oncology030220 oncology & carcinogenesisColonic NeoplasmsFemaleOligopeptidesSignal Transductionmedicine.medical_specialtyProgrammed cell deathBlotting WesternMolecular Sequence DataMice Nude[SDV.CAN]Life Sciences [q-bio]/CancerCell Line03 medical and health sciencesIn vivoInternal medicinemedicineAnimalsHumansAmino Acid Sequence030304 developmental biologybusiness.industrySurface Plasmon ResonanceHCT116 CellsAntineoplastic Agents PhytogenicXenograft Model Antitumor AssaysIn vitroReceptors TNF-Related Apoptosis-Inducing LigandEndocrinologyResveratrolCell cultureApoptosisCancer cellCancer researchbusiness
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Biological indicators of prognosis in Ewing's sarcoma: An emerging role for lectin galactoside-binding soluble 3 binding protein (LGALS3BP)

2009

Starting from an experimental model that accounts for the 2 most important adverse processes to successful therapy of Ewing's sarcoma (EWS), chemoresistance and the presence of metastasis at the time of diagnosis, we defined a molecular signature of potential prognostic value. Functional annotation of differentially regulated genes revealed 3 major networks related to cell cycle, cell-to-cell interactions and cellular development. The prognostic impact of 8 genes, representative of these 3 networks, was validated in 56 EWS patients. High mRNA expression levels of HINT1, IFITM2, LGALS3BP, STOML2 and c-MYC were associated with reduced risk to death and lower risk to develop metastasis. At mul…

Cancer ResearchMice NudeEnzyme-Linked Immunosorbent AssaySarcoma EwingBiologyMetastasisMiceAntigens NeoplasmCell Line TumorBiomarkers TumorCell AdhesionmedicineAnimalsHumansGene SilencingRNA MessengerNeoplasm MetastasisGlycoproteinsOligonucleotide Array Sequence AnalysisTumor microenvironmentReverse Transcriptase Polymerase Chain ReactionCell CycleMatricellular proteinEwing's sarcomaCell cyclePrognosismedicine.diseaseImmunohistochemistryOncologyTumor progressionImmunologyGalactoside bindingCancer researchSarcomaCarrier ProteinsSignal TransductionInternational Journal of Cancer
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Nanofitins targeting heat shock protein 110: an innovative immunotherapeutic modality in cancer.

2021

The presence of an inactivating heat shock protein 110 (HSP110) mutation in colorectal cancers has been correlated with an excellent prognosis and with the ability of HSP110 to favor the formation of tolerogenic (M2-like) macrophages. These clinical and experimental results suggest a potentially powerful new strategy against colorectal cancer: the inhibition of HSP110. In this work, as an alternative to neutralizing antibodies, Nanofitins (scaffold ~7 kDa proteins) targeting HSP110 were isolated from the screening of a synthetic Nanofitin library, and their capacity to bind (immunoprecipitation, biolayer interferometry) and to inhibit HSP110 was analyzed in vitro and in vivo. Three Nanofiti…

Cancer ResearchMice03 medical and health sciencesLymphocytes Tumor-Infiltrating0302 clinical medicineImmune systemPeptide LibraryIn vivoCell Line TumorHeat shock proteinTumor MicroenvironmentmedicineAnimalsHumansCytotoxic T cellHSP110 Heat-Shock Proteinssmall peptide moleculesTumor microenvironmentanticancer targeted therapybiologyChemistryMacrophagesCancer[SDV.SP]Life Sciences [q-bio]/Pharmaceutical sciencesmedicine.diseaseXenograft Model Antitumor AssaysPeptide FragmentsIn vitro3. Good healthNanofitinsOncologyPositron-Emission Tomography030220 oncology & carcinogenesisbiology.proteinCancer researchFemaleAntibodyColorectal NeoplasmsHSP110
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Inhibition of human immunodeficiency virus-1 infection by human conglutinin-like protein: in vitro studies.

1992

The lectin-like protein analogous to bovine conglutinin was purified from human serum. The carbohydrate-binding ability of conglutinin-like protein was inhibited by D-mannose, N-acetylglucosamine and L-fucose as well as by mannan-containing oligosaccharides. By applying a lectin-based ELISA system it was demonstrated that conglutinin-like protein binds to human immunodeficiency virus-1 (HIV-1) glycoprotein 120 (gp120) via its carbohydrate binding site. In vitro experiments with T-lymphoblastoid CEM cells revealed that conglutinin-like protein abolishes infection by HIV-1; a 50% cytoprotective concentration of 23.9 micrograms/ml was measured. These findings demonstrate that human conglutinin…

Cancer ResearchMolecular Sequence DataCarbohydratesImmunoglobulinsEnzyme-Linked Immunosorbent AssayHIV Envelope Protein gp120Mannose-Binding LectinVirusChromatography AffinityArticleViral ProteinsConglutininProtein A/GHumansImmunoconglutininsBinding siteKey wordsConglutinin‐like proteinchemistry.chemical_classificationAcquired Immunodeficiency SyndromebiologyHIV‐1Immunization PassiveLectinMolecular biologyMannanIn vitrogp120OncologychemistryCarbohydrate Sequencebiology.proteinHIV-1Protein GGlycoproteinCarrier ProteinsLectinJapanese journal of cancer research : Gann
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WIN induces apoptotic cell death in human colon cancer cells through a block of autophagic flux dependent on PPARγ down-regulation.

2014

Cannabinoids have been reported to possess anti-tumorigenic activity in cancer models although their mechanism of action is not well understood. Here, we show that the synthetic cannabinoid WIN55,212-2 (WIN)-induced apoptosis in colon cancer cell lines is accompanied by endoplasmic reticulum stress induction. The formation of acidic vacuoles and the increase in LC3-II protein indicated the involvement of autophagic process which seemed to play a pro-survival role against the cytotoxic effects of the drug. However, the enhanced lysosomal membrane permeabilization (LMP) blocked the autophagic flux after the formation of autophagosomes as demonstrated by the accumulation of p62 and LC3, two ma…

Cancer ResearchMorpholinesClinical BiochemistryPharmaceutical ScienceDown-RegulationAntineoplastic AgentsApoptosisBiologyNaphthalenesDownregulation and upregulationSettore BIO/10 - BiochimicaCell Line TumormedicineAutophagyGene silencingHumansViability assayPharmacologyEndoplasmic reticulumBiochemistry (medical)AutophagyCannabinoids PPARγ ER stress autophagy/apoptosis interplay colon carcinoma cellsCell BiologyEndoplasmic Reticulum StressCell biologyBenzoxazinesMitochondriaPPAR gammaMechanism of actionApoptosisColonic NeoplasmsUnfolded protein responsemedicine.symptomSignal TransductionApoptosis : an international journal on programmed cell death
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XPO1E571K Mutation Modifies Exportin 1 Localisation and Interactome in B-cell Lymphoma

2020

The XPO1 gene encodes exportin 1 (XPO1) that controls the nuclear export of cargo proteins and RNAs. Almost 25% of primary mediastinal B-cell lymphoma (PMBL) and classical Hodgkin lymphoma (cHL) cases harboured a recurrent XPO1 point mutation (NM_003400, chr2:g61718472C&gt

Cancer ResearchMutantXPO1/CRM1[SDV.CAN]Life Sciences [q-bio]/Cancer[SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]CRISPR–Cas9[SDV.BC.IC] Life Sciences [q-bio]/Cellular Biology/Cell Behavior [q-bio.CB]lcsh:RC254-282Article03 medical and health sciencesXPO10302 clinical medicineproteomics[SDV.CAN] Life Sciences [q-bio]/Cancerimmune system diseasesExportin-1hemic and lymphatic diseases[SDV.BC.IC]Life Sciences [q-bio]/Cellular Biology/Cell Behavior [q-bio.CB]medicine[SDV.BC.BC] Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]B-cell lymphomaNuclear export signalproximity ligation assay030304 developmental biology0303 health sciencesimportin β1ChemistryB-cell lymphomaPoint mutationlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseMolecular biologynuclear importindirect immunofluorescenceOncology030220 oncology & carcinogenesisMutation (genetic algorithm)nuclear exportNuclear transportCRISPR-Cas9
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