Search results for "Apoptosis."

showing 10 items of 1794 documents

Apoptotic effects of thiazolobenzimidazole derivatives on sensitive and multidrug resistant leukaemic cells

2001

We investigated the cytotoxic activity of eight thiazolobenzimidazole derivatives on sensitive HL60 and multidrug-resistant (MDR) (HL60R) leukaemia cell lines. The antitumour effects of these compounds were compared with those of RS-TBZ, a thiazolobenzimidazole derivative, previously described in our reports, that was able to induce apoptosis more markedly in MDR cells than in the parental sensitive cell lines. Only two compounds in this study proved to have interesting effects: (a) the S-enantiomer of TBZ, that was able to induce apoptosis in MDR cells in a slightly more selective manner than TBZ (racemic form); and (b) TBZ-4-OCH3 (TBZ-4-OCH3), that showed cytotoxic and apoptotic effects o…

Cancer ResearchHL60Antineoplastic AgentsHL-60 CellsApoptosisBiologyMultidrug resistanceCaspase 8Anticancer drugschemistry.chemical_compoundAntigenCytotoxic T cellHumansLeukaemiafas ReceptorProgenitor cellLeukemiaCell CycleCaspase InhibitorsDrug Resistance MultipleMultiple drug resistanceThiazolobenzimidazoleThiazolesAnticancer drugs; Apoptosis; Leukaemia; Multidrug resistance; Thiazolobenzimidazole;OncologychemistryCell cultureApoptosisDrug Resistance NeoplasmImmunologyCancer researchBenzimidazoles
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Autophagy and mitochondrial alterations in human retinal pigment epithelial cells induced by ethanol: implications of 4-hydroxy-nonenal

2014

Retinal pigment epithelium has a crucial role in the physiology and pathophysiology of the retina due to its location and metabolism. Oxidative damage has been demonstrated as a pathogenic mechanism in several retinal diseases, and reactive oxygen species are certainly important by-products of ethanol (EtOH) metabolism. Autophagy has been shown to exert a protective effect in different cellular and animal models. Thus, in our model, EtOH treatment increases autophagy flux, in a concentration-dependent manner. Mitochondrial morphology seems to be clearly altered under EtOH exposure, leading to an apparent increase in mitochondrial fission. An increase in 2′,7′-dichlorofluorescein fluorescenc…

Cancer ResearchImmunologyApoptosisRetinal Pigment EpitheliumMitochondrionBiologymedicine.disease_causeCell LineLipid peroxidationCellular and Molecular Neurosciencechemistry.chemical_compoundRetinal DiseasesmedicineAutophagyHumanschemistry.chemical_classificationReactive oxygen speciesAldehydesRetinal pigment epitheliumEthanolAutophagyRetinalEpithelial CellsCell BiologyCell biologyMitochondriaOxidative Stressmedicine.anatomical_structurechemistryBiochemistryMitochondrial fissionOriginal ArticleReactive Oxygen SpeciesOxidative stressCell Death & Disease
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Moguntinones--new selective inhibitors for the treatment of human colorectal cancer.

2014

Abstract 3-Indolyl and 3-azaindolyl-4-aryl maleimide derivatives, called moguntinones (MOG), have been selected for their ability to inhibit protein kinases associated with angiogenesis and induce apoptosis. Here, we characterize their mode of action and their potential clinical value in human colorectal cancer in vitro and in vivo. MOG-19 and MOG-13 were characterized in vitro using kinase, viability, and apoptosis assays in different human colon cancer (HT-29, HCT-116, Caco-2, and SW480) and normal colon cell lines (CCD-18Co, FHC, and HCoEpiC) alone or in combination with topoisomerase I inhibitors. Intracellular signaling pathways were analyzed by Western blotting. To determine their pot…

Cancer ResearchIndolesColorectal cancerAngiogenesisApoptosisBiologyPharmacologyMetastasisMaleimidesMiceIn vivomedicineAnimalsHumansPI3K/AKT/mTOR pathwayKinaseTOR Serine-Threonine Kinasesmedicine.diseaseXenograft Model Antitumor AssaysOncologyApoptosisSignal transductionCaco-2 CellsTopoisomerase I InhibitorsColorectal NeoplasmsHT29 CellsProto-Oncogene Proteins c-aktSignal TransductionMolecular cancer therapeutics
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Selectivity analysis of protein kinase CK2 inhibitors DMAT, TBB and resorufin in cisplatin-induced stress responses.

2009

Udgivelsesdato: 2009-Nov Targeting protein kinases as a therapeutic approach to treat various diseases, especially cancer is currently a fast growing business. Although many inhibitors are available, exhibiting remarkable potency, the major challenge is their selectivity. Here we show that the protein kinase CK2 inhibitors DMAT, TBB and resorufin differ in their selectivity against PI3K family members, since PI3K and DNA-PK are subject to inhibition by DMAT and TBB, however, not by resorufin. TBB and DMAT treatment together with cisplatin lead to an inhibition of cisplatin-induced stress signaling (as detected by phosphorylation of JNK and H2AX). In the case of resorufin no interference wit…

Cancer ResearchKinaseCell SurvivalBlotting WesternAntineoplastic AgentsCell cycleBiologyTriazolesCell killingOncologyBiochemistryApoptosisStress PhysiologicalCell Line TumorOxazinesPhosphorylationHumansBenzimidazolesViability assayCasein kinase 2Signal transductionCisplatinEnzyme InhibitorsCasein Kinase IISignal TransductionInternational journal of oncology
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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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Efficacy of BET Bromodomain Inhibition in Kras-Mutant Non–Small Cell Lung Cancer

2013

Abstract Purpose: Amplification of MYC is one of the most common genetic alterations in lung cancer, contributing to a myriad of phenotypes associated with growth, invasion, and drug resistance. Murine genetics has established both the centrality of somatic alterations of Kras in lung cancer, as well as the dependency of mutant Kras tumors on MYC function. Unfortunately, drug-like small-molecule inhibitors of KRAS and MYC have yet to be realized. The recent discovery, in hematologic malignancies, that bromodomain and extra-terminal (BET) bromodomain inhibition impairs MYC expression and MYC transcriptional function established the rationale of targeting KRAS-driven non–small cell lung cance…

Cancer ResearchLKB1Lung NeoplasmsMutantApoptosisMYCAMP-Activated Protein KinasesProtein Serine-Threonine KinasesBiologyNSCLCmedicine.disease_causeArticleProto-Oncogene Proteins c-mycProto-Oncogene Proteins p21(ras)MiceRNA interferenceCarcinoma Non-Small-Cell LungCell Line TumorKRASmedicineAnimalsRNA Small InterferingLung cancerneoplasmsCell ProliferationMice KnockoutGene knockdownCell growthNuclear ProteinsCancerAzepinesTriazolesBETmedicine.diseaseMolecular biologydigestive system diseasesrespiratory tract diseasesBromodomainOncologyCancer researchRNA InterferenceKRASSignal TransductionTranscription FactorsClinical Cancer Research
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cIAP1 regulates TNF-mediated cdc42 activation and filopodia formation

2013

International audience; umour necrosis factor-α (TNF) is a cytokine endowed with multiple functions, depending on the cellular and environmental context. TNF receptor engagement induces the formation of a multimolecular complex including the TNFR-associated factor TRAF2, the receptor-interaction protein kinase RIP1 and the cellular inhibitor of apoptosis cIAP1, the latter being essential for NF-κB activation. Here, we show that cIAP1 also regulates TNF-induced actin cytoskeleton reorganization through a cdc42-dependent, NF-κB-independent pathway. Deletion of cIAP1 prevents TNF-induced filopodia and cdc42 activation. The expression of cIAP1 or its E3-ubiquitin ligase-defective mutant restore…

Cancer ResearchLung NeoplasmsBlotting WesternFluorescent Antibody Techniquemacromolecular substancesCDC42BiologyTransfectionInhibitor of Apoptosis ProteinsMice03 medical and health sciences0302 clinical medicineCell AdhesionGeneticsAnimalsHumansImmunoprecipitationNeoplasm InvasivenessPseudopodia[SPI.NANO]Engineering Sciences [physics]/Micro and nanotechnologies/Microelectronicscdc42 GTP-Binding ProteinMolecular Biology030304 developmental biology0303 health sciencesTumor Necrosis Factor-alphaActin cytoskeleton reorganizationCell PolarityActin remodelingSurface Plasmon ResonanceActin cytoskeletonCell biologyActin CytoskeletonDisease Models AnimalHEK293 CellsCdc42 GTP-Binding Protein030220 oncology & carcinogenesisNIH 3T3 CellsHeterografts[ SPI.NANO ] Engineering Sciences [physics]/Micro and nanotechnologies/MicroelectronicsPseudopodiaSignal transductionFilopodiaSignal TransductionOncogene
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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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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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Breast cancer genome-wide association studies: there is strength in numbers.

2012

Breast cancer (BC) is a heterogeneous disease that exhibits familial aggregation. Family linkage studies have identified high-penetrance genes, BRCA1, BRCA2, PTEN and TP53, that are responsible for inherited BC syndromes. Moreover, a combination of family-based and population-based approaches indicated that genes involved in DNA repair, such as CHEK2, ATM, BRIP and PALB2, are associated with moderate risk. Therefore, all of these known genes account for only 25% of the familial aggregation cases. Recently, genome wide association studies (GWAS) in BC revealed single nucleotide polymorphisms (SNPs) in five novel genes associated to susceptibility: TNRC9, FGFR2, MAP3K1, H19 and lymphocyte-spe…

Cancer ResearchMultifactorial InheritanceSettore MED/06 - Oncologia MedicaPALB2PopulationMAP Kinase Kinase Kinase 1Single-nucleotide polymorphismGenome-wide association studyBreast NeoplasmsBiologyPolymorphism Single NucleotideGenetic linkageGeneticsSNPHumansGenetic Predisposition to DiseaseReceptor Fibroblast Growth Factor Type 2educationMolecular BiologyGeneCHEK2Geneticsbreast cancer GWASeducation.field_of_studyMicrofilament ProteinsHigh Mobility Group ProteinsCancer researchTrans-ActivatorsFemaleApoptosis Regulatory ProteinsReceptors ProgesteroneGenome-Wide Association StudyOncogene
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