Search results for "APOPTOSIS"

showing 10 items of 1809 documents

Inhibitory Effect of Kurarinone on Growth of Human Non-small Cell Lung Cancer: An Experimental Study Both in Vitro and in Vivo Studies

2018

Kurarinone, a flavonoid isolated from Sophora flavescens Aiton, has been reported to have significant antitumor activity. However, the cytotoxic activity of kurarinone against non-small cell lung cancer (NSCLC) cells is still under explored. In our study, we have evaluated the inhibitory effects of kurarinone on the growth of NSCLC both in vivo and in vitro as well as the molecular mechanisms underlying kurarinone-induced A549 cell apoptosis. The results showed that kurarinone effectively inhibited the proliferation of A549 cells with little toxic effects on human bronchial epithelial cell line BEAS-2B. FASC examination and Hoechst 33258 staining assay showed that kurarinone dose-dependentl…

0301 basic medicineCaspase 303 medical and health sciences0302 clinical medicineIn vivoCytotoxic T cellPharmacology (medical)Protein kinase BPharmacologyA549 cellCaspase-9biologyChemistrymulti-targetlcsh:RM1-950apoptosiskurarinoneIn vitrorespiratory tract diseases030104 developmental biologyanticancer activitylcsh:Therapeutics. PharmacologyApoptosis030220 oncology & carcinogenesisCancer researchbiology.proteinlung carcinomaFrontiers in Pharmacology
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Study of novel anticancer 4-thiazolidinone derivatives

2016

Abstract 4-Thiazolidinones are a known class of prospective drug-like molecules, especially in the design of new anticancer agents. Two of the most prominent subtypes of these compounds are 5-ene-2-amino(amino)-4-thiazolidinones and thiopyrano[2,3-d]thiazoles. The latter are considered to be cyclic mimetics of biologically active 5-ene-4-thiazolidinones with similar pharmacological profiles. Therefore, the aim of this study was to evaluate the impact of 4-thiazolidinone-based compounds on cytotoxicity, the apoptotic process, and metabolism in the human squamous carcinoma (SCC-15) cell line. The SCC-15 cells were cultured in phenol red-free DMEM/F12 medium supplemented with 10% FBS, hydrocor…

0301 basic medicineCell SurvivalCytotoxicityAntineoplastic AgentsApoptosisToxicology01 natural sciencesAnticancer activity03 medical and health sciencesCell Line TumormedicineHumansViability assayCytotoxicitychemistry.chemical_classificationReactive oxygen speciesL-Lactate Dehydrogenase010405 organic chemistryChemistryCaspase 3ThiazolothiopyranesBiological activityGeneral MedicineMetabolism0104 chemical sciencesSquamous carcinomaThiazoles030104 developmental biologyMechanism of actionBiochemistryMicroscopy FluorescenceCell cultureThiazolidinonemedicine.symptomReactive Oxygen SpeciesChemico-Biological Interactions
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Extracellular histones activate autophagy and apoptosis via mTOR signaling in human endothelial cells.

2018

Circulating histones have been proposed as targets for therapy in sepsis and hyperinflammatory symptoms. However, the proposed strategies have failed in clinical trials. Although different mechanisms for histone-related cytotoxicity are being explored, those mediated by circulating histones are not fully understood. Extracellular histones induce endothelial cell death, thereby contributing to the pathogenesis of complex diseases such as sepsis and septic shock. Therefore, the comprehension of cellular responses triggered by histones is capital to design effective therapeutic strategies. Here we report how extracellular histones induce autophagy and apoptosis in a dose-dependent manner in cu…

0301 basic medicineCell SurvivalEndothelial cellsFisiologiaApoptosisAMP-Activated Protein KinasesHistones03 medical and health sciencesExtracellularAutophagyHuman Umbilical Vein Endothelial CellsAutophagy-Related Protein-1 HomologHumansMolecular BiologyProtein kinase BPI3K/AKT/mTOR pathwaybiologyDose-Response Relationship DrugChemistryTOR Serine-Threonine KinasesAutophagyIntracellular Signaling Peptides and ProteinsAMPKNuclear ProteinsCirculating histonesCell biologyToll-like receptorsEndothelial stem cell030104 developmental biologyHistoneApoptosisbiology.proteinMolecular MedicineProto-Oncogene Proteins c-aktSignal TransductionBiochimica et biophysica acta. Molecular basis of disease
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Indomethacin Disrupts Autophagic Flux by Inducing Lysosomal Dysfunction in Gastric Cancer Cells and Increases Their Sensitivity to Cytotoxic Drugs

2018

AbstractNSAIDs inhibit tumorigenesis in gastrointestinal tissues and have been proposed as coadjuvant agents to chemotherapy. The ability of cancer epithelial cells to adapt to the tumour environment and to resist cytotoxic agents seems to depend on rescue mechanisms such as autophagy. In the present study we aimed to determine whether an NSAID with sensitizing properties such as indomethacin modulates autophagy in gastric cancer epithelial cells. We observed that indomethacin causes lysosomal dysfunction in AGS cells and promotes the accumulation of autophagy substrates without altering mTOR activity. Indomethacin enhanced the inhibitory effects of the lysosomotropic agent chloroquine on l…

0301 basic medicineCell SurvivalIndomethacinlcsh:MedicineAntineoplastic AgentsAdenocarcinomaArticle03 medical and health sciencesStomach NeoplasmsCell Line TumorLysosomeAutophagymedicineHumansCytotoxic T cellViability assayCytotoxicitylcsh:SciencePI3K/AKT/mTOR pathwayAnalysis of VarianceMultidisciplinaryCell DeathChemistryAnti-Inflammatory Agents Non-SteroidalAutophagylcsh:RChloroquineDrug SynergismOxaliplatin030104 developmental biologymedicine.anatomical_structureDrug Resistance NeoplasmApoptosisCancer cellCancer researchlcsh:QMacrolidesLysosomesScientific Reports
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Beauvericin and enniatin B effects on a human lymphoblastoid Jurkat T-cell model

2018

Abstract Several mycotoxins exert their effect on the immunological system; some are classified as immunotoxic. Jurkat T-cells were used to study toxic effects of beauvericin (BEA) and enniatin B (ENN B). Both are not legislated mycotoxins with increasing presence in feed and food. Concentrations studied were from 1 to 15 μM at 24, 48 and 72 h. Cell death by increasing the percentage of apoptotic/necrotic cells was: BEA > ENN B. IC50 values ranged from 3 to 7.5 μM for BEA. ENN B 15 μM decreased viability (21-29%). The percentage of apoptotic/necrotic cells was BEA > ENN B at 24 h but not at 48 h. Caspase-3&7 activation profile varied, although both mycotoxins increased this activation. No d…

0301 basic medicineCell SurvivalT-LymphocytesT cellApoptosisToxicologyJurkat cells03 medical and health scienceschemistry.chemical_compound0404 agricultural biotechnologyDepsipeptidesmedicineHumansMycotoxinCytotoxicityCaspase 7Caspase 3LymphoblastCell Cycle04 agricultural and veterinary sciencesGeneral MedicineMycotoxins040401 food scienceMolecular biologyBeauvericin030104 developmental biologymedicine.anatomical_structurechemistryApoptosisToxicityFood ScienceFood and Chemical Toxicology
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Chemopreventive Property of Sencha Tea Extracts towards Sensitive and Multidrug-Resistant Leukemia and Multiple Myeloma Cells

2020

The popular beverage green tea possesses chemopreventive activity against various types of tumors. However, the effects of its chemopreventive effect on hematological malignancies have not been defined. In the present study, we evaluated antitumor efficacies of a specific green tea, sencha tea, on sensitive and multidrug-resistant leukemia and a panel of nine multiple myelomas (MM) cell lines. We found that sencha extracts induced cytotoxicity in leukemic cells and MM cells to different extents, yet its effect on normal cells was limited. Furthermore, sencha extracts caused G2/M and G0/G1 phase arrest during cell cycle progression in CCRF/CEM and KMS-12-BM cells, respectively. Specifically,…

0301 basic medicineCell Survivalnatural productsgreen tealcsh:QR1-502Cell morphologychemotherapyBiochemistryArticlelcsh:Microbiologyfunctional foodPhosphatidylinositol 3-Kinases03 medical and health sciences0302 clinical medicineCell Line TumorHumansCytotoxicityMolecular BiologyProtein kinase BcatechinsPI3K/AKT/mTOR pathwaypolyphenolsCell ProliferationMembrane Potential MitochondrialLeukemiadrug resistanceTeaPlant ExtractsChemistryCell growthCell CycleNF-kappa BCell cycleAntineoplastic Agents PhytogenicDrug Resistance MultipleGene Expression Regulation Neoplastic030104 developmental biologyDrug Resistance NeoplasmApoptosisCell culture030220 oncology & carcinogenesisflavonoidsCancer researchmicroarray analysisMultiple MyelomaReactive Oxygen SpeciesProto-Oncogene Proteins c-aktSignal TransductionBiomolecules
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Physiological concentrations of phytosterols enhance the apoptotic effects of 5-fluorouracil in colon cancer cells

2018

Abstract Combining natural products as co-adjuvants in 5-fluorouracil (5-FU) chemotherapy might enhance the effectiveness of 5-FU by avoiding a high dosage and/or reducing treatment times. We explored the anticancer efficacy of the phytosterols (PS) at concentrations achievable in the human colon, as well as their potential as sensitizing agents of human colon cancer cells (Caco-2 and HT-29) to 5-FU treatment. Cells proliferation, combination index, cell cycle, apoptosis, caspases activation, ROS production, and ΔΨm were determined. Co-treatment (PS+5-FU) had an antiproliferative additive effect, and moreover, in general a significantly improved efficacy was observed on cell cycle arrest at…

0301 basic medicineCell cycle checkpointColorectal cancermedicine.medical_treatmentMedicine (miscellaneous)ApoptosisCell cycle03 medical and health sciences0302 clinical medicineIn vivomedicine5-fluorouracilTX341-641Colon cancer cellsCaspaseChemotherapyNutrition and DieteticsbiologyNutrition. Foods and food supplyChemistryPhytosterolsCell cyclemedicine.disease030104 developmental biologyApoptosisFluorouracil030220 oncology & carcinogenesisCancer researchbiology.proteinDrug sensitivityFood Sciencemedicine.drugJournal of Functional Foods
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[1,2]Oxazolo[5,4-e]isoindoles as promising tubulin polymerization inhibitors

2016

Abstract A series of [1,2]Oxazolo [5,4- e ]isoindoles has been synthesized through a versatile and high yielding sequence. All the new structures showed in the 1 HNMR spectra, the typical signal in the 8.34–8.47 ppm attributable to the H-3 of the [1,2]oxazole moiety. Among all derivatives, methoxy benzyl substituents at positions 3 and 4 or/and 5 were very effective in reducing the growth of different tumor cell lines, including diffuse malignant peritoneal mesothelioma (DMPM), an uncommon and rapidly malignancy poorly responsive to available therapeutic options. The most active compound 6j was found to impair tubulin polymerization, cause cell cycle arrest at G2/M phase and induce apoptosi…

0301 basic medicineCell cycle checkpointIsoindoles2]Oxazolo[5StereochemistryDiffuse malignant peritoneal mesotheliomaα-hydroxyalkyl ketonesAntineoplastic AgentsApoptosisIsoindoles01 natural sciencesTubulin Polymerization Inhibitors03 medical and health scienceschemistry.chemical_compoundIsomerismTubulinCell Line TumorDrug DiscoveryHumansMoietyProtein Structure QuaternaryOxazole[12]Oxazolo[54-e]isoindolePharmacology010405 organic chemistryChemistryAntitubulin agentsDrug Discovery3003 Pharmaceutical ScienceOrganic ChemistryGeneral MedicineSettore CHIM/08 - Chimica FarmaceuticaTubulin Modulators0104 chemical sciencesAntitubulin agentG2 Phase Cell Cycle Checkpointsα-hydroxyalkyl ketone030104 developmental biologyApoptosisActive compound4-e]isoindolesProton NMRM Phase Cell Cycle CheckpointsAntitubulin agents; Diffuse malignant peritoneal mesothelioma; [1; 2]Oxazolo[5; 4-e]isoindoles; α-hydroxyalkyl ketones; Pharmacology; Drug Discovery3003 Pharmaceutical Science; Organic Chemistry[1Drug Screening Assays AntitumorProtein Multimerization
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Carob leaf polyphenols trigger intrinsic apoptotic pathway and induce cell cycle arrest in colon cancer cells

2017

IF 3.973; International audience; Chemoprevention of Colorectal cancer (CRC) is the major concern for improving public health. We investigated the protective effects of carob, Ceratonia siliqua L, leaf polyphenols (CLP) against CRC. Phenolic content analysis showed that CLP is enriched with gallic acid and m-coumaric acid. We observed that CLP exerted a dose dependent cytotoxic effect through the induction of apoptosis on CRC cell lines, with an IC50 around 20 mu g/mL CLP induced intrinsic apoptotic pathway through the caspase-9 activation and PARP cleavage in HCT-116 and CT-26 cells. Moreover, CLP induced cell cycle arrest in the G1 phase through p53 activation. Gallic acid and m-coumaric …

0301 basic medicineCell cycle checkpointanimal diseases[ SDV.AEN ] Life Sciences [q-bio]/Food and NutritionMedicine (miscellaneous)ApoptosisPharmacologydigestive systemCell cycle arrest03 medical and health scienceschemistry.chemical_compoundCytotoxic T cellTX341-641Gallic acidIC50CaspaseNutrition and DieteticsbiologyNutrition. Foods and food supplyChemistryCarob (Ceratonia siliqua L.)food and beveragesPolyphenolsbacterial infections and mycosesColorectal cancer3. Good healthstomatognathic diseases030104 developmental biologyBiochemistryCell cultureApoptosisPolyphenolCaspasesbiology.protein[SDV.AEN]Life Sciences [q-bio]/Food and NutritionFood Science
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Integrated molecular signaling involving mitochondrial dysfunction and alteration of cell metabolism induced by tyrosine kinase inhibitors in cancer.

2020

Cancer cells have unlimited replicative potential, insensitivity to growth-inhibitory signals, evasion of apoptosis, cellular stress, and sustained angiogenesis, invasiveness and metastatic potential. Cancer cells adequately adapt cell metabolism and integrate several intracellular and redox signaling to promote cell survival in an inflammatory and hypoxic microenvironment in order to maintain/expand tumor phenotype. The administration of tyrosine kinase inhibitor (TKI) constitutes the recommended therapeutic strategy in different malignancies at advanced stages. There are important interrelationships between cell stress, redox status, mitochondrial function, metabolism and cellular signali…

0301 basic medicineCell deathCell signalingClinical BiochemistryPGC-1αApoptosisReview ArticleBiochemistryReceptor tyrosine kinase03 medical and health sciencesPhosphatidylinositol 3-Kinases0302 clinical medicineNeoplasmsAutophagyTumor MicroenvironmentHumansProtein kinase AProtein kinase Blcsh:QH301-705.5Protein Kinase InhibitorsPI3K/AKT/mTOR pathwaylcsh:R5-920biologyOrganic ChemistryMitochondria030104 developmental biologylcsh:Biology (General)Redox statusCancer cellbiology.proteinCancer researchEndoplasmic reticulum stressmTORSignal transductionlcsh:Medicine (General)Tyrosine kinaseProto-Oncogene Proteins c-akt030217 neurology & neurosurgeryRedox biology
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