Search results for "Cell Cycle Checkpoints"

showing 10 items of 67 documents

Silymarin and Cancer: A Dual Strategy in Both in Chemoprevention and Chemosensitivity

2020

Silymarin extracted from milk thistle consisting of flavonolignan silybin has shown chemopreventive and chemosensitizing activity against various cancers. The present review summarizes the current knowledge on the potential targets of silymarin against various cancers. Silymarin may play on the system of xenobiotics, metabolizing enzymes (phase I and phase II) to protect normal cells against various toxic molecules or to protect against deleterious effects of chemotherapeutic agents on normal cells. Furthermore, silymarin and its main bioactive compounds inhibit organic anion transporters (OAT) and ATP-binding cassettes (ABC) transporters, thus contributing to counteracting potential chemor…

Programmed cell deathsilymarinCellChemosensitizerPharmaceutical SciencechemopreventiveATP-binding cassette transporterApoptosisReviewProtective AgentsChemopreventionsilybinAnalytical Chemistrylcsh:QD241-44103 medical and health sciences0302 clinical medicinelcsh:Organic chemistryDrug DiscoverymedicineHumansPhysical and Theoretical ChemistryReceptor030304 developmental biology0303 health sciencesChemistryOrganic ChemistryCancerCell Cycle CheckpointsCell cyclemedicine.diseasemedicine.anatomical_structureChemistry (miscellaneous)intrinsic and extrinsic pathwayDrug Resistance Neoplasm030220 oncology & carcinogenesisCancer cellchemosensitizerCancer researchMolecular Medicinemetabolizing enzymesATP-Binding Cassette Transporterscell cycleABC transporterSignal TransductionMolecules
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Bioinformatic and experimental fishing for artemisinin-interacting proteins from human nasopharyngeal cancer cells.

2012

Determining interacting cellular partners of drugs by chemical proteomic techniques is complex and tedious. Most approaches rely on activity-based probe profiling and compound-centric chemical proteomics. The anti-malarial artemisinin also exerts profound anti-cancer activity, but the mechanisms of action are incompletely understood. In the present investigation, we present a novel approach to identify artemisinin-interacting target proteins. Our approach overcomes usual problems in traditional fishing procedures, because the drug was attached to a surface without further chemical modification. The proteins identified effect among others, cell cycle arrest, apoptosis, inhibition of angiogen…

ProteomicsCell cycle checkpointCell growthAngiogenesisComputational BiologyCell migrationApoptosisNasopharyngeal NeoplasmsCell Cycle CheckpointsBiologyProteomicsArtemisininsCell biologyNeoplasm ProteinsNuclear receptorCell cultureCell Line TumormedicineAnticarcinogenic AgentsHumansArtemisininMolecular BiologyBiotechnologymedicine.drugCell ProliferationMolecular bioSystems
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Piclamilast inhibits the pro-apoptotic and anti-proliferative responses of A549 cells exposed to H(2)O(2) via mechanisms involving AP-1 activation.

2012

Reactive oxygen species (ROS) are involved in the pathogenesis of many inflammatory diseases such as chronic obstructive pulmonary disease (COPD). They can alter the expression of genes involved in cellular damage by activating transcription factors, including the NF-κB and the activator protein 1 (AP-1). Phosphodiesterase type 4 (PDE4) inhibitors have anti-inflammatory and antioxidant effects, as described in in vivo and in vitro COPD models. This study analysed the effects of piclamilast, a selective PDE4 inhibitor, on modulating the global gene expression profile in A549 cells exposed to H(2)O(2).Changes in gene expression were analysed using high-density Affymetrix microarrays and valid…

Proto-Oncogene Proteins c-junPyridinesActivating transcription factorApoptosisBiologymedicine.disease_causeBiochemistryAntioxidantschemistry.chemical_compoundPulmonary Disease Chronic ObstructiveIn vivoAnnexinCell Line TumorGene expressionmedicineHumansRNA MessengerPhosphorylationCell ProliferationOligonucleotide Array Sequence AnalysisA549 cellGene Expression ProfilingNF-kappa BGeneral MedicineCell Cycle CheckpointsHydrogen PeroxideMolecular biologyTranscription Factor AP-1chemistryGene Expression RegulationAlveolar Epithelial CellsBenzamidesPhosphodiesterase 4 InhibitorsSignal transductionReactive Oxygen SpeciesPiclamilastOxidative stressSignal TransductionFree radical research
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The endoperoxide ascaridol shows strong differential cytotoxicity in nucleotide excision repair-deficient cells

2011

Targeting synthetic lethality in DNA repair pathways has become a promising anti-cancer strategy. However little is known about such interactions with regard to the nucleotide excision repair (NER) pathway. Therefore, cell lines with a defect in the NER genes ERCC6 or XPC and their normal counterparts were screened with 53 chemically defined phytochemicals isolated from plants used in traditional Chinese medicine for differential cytotoxic effects. The screening revealed 12 drugs that killed NER-deficient cells more efficiently than proficient cells. Five drugs were further analyzed for IC50 values, effects on cell cycle distribution, and induction of DNA damage. Ascaridol was the most effe…

RAD23BDNA RepairDNA repairDNA damageCyclohexane MonoterpenesBiologyToxicologyCell LineInhibitory Concentration 50HumansCytotoxic T cellMedicine Chinese TraditionalPharmacologyDose-Response Relationship DrugCell cycleAntineoplastic Agents PhytogenicMolecular biologyPeroxidesG2 Phase Cell Cycle CheckpointsCell cultureCancer cellMonoterpenesM Phase Cell Cycle CheckpointsReactive Oxygen SpeciesDNA DamageDrugs Chinese HerbalNucleotide excision repairToxicology and Applied Pharmacology
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DNA damage causes TP53-dependent coupling of self-renewal and senescence pathways in embryonal carcinoma cells.

2013

Recent studies have highlighted an apparently paradoxical link between self-renewal and senescence triggered by DNA damage in certain cell types. In addition, the finding that TP53 can suppress senescence has caused a re-evaluation of its functional role in regulating these outcomes. To investigate these phenomena and their relationship to pluripotency and senescence, we examined the response of the TP53-competent embryonal carcinoma (EC) cell line PA-1 to etoposide-induced DNA damage. Nuclear POU5F1/OCT4A and P21CIP1 were upregulated in the same cells following etoposide-induced G 2M arrest. However, while accumulating in the karyosol, the amount of OCT4A was reduced in the chromatin fract…

SenescenceCyclin-Dependent Kinase Inhibitor p21OCT4A/POU5F1Embryonal Carcinoma Stem CellssenescenceDNA RepairDNA repairDNA damagetumor cellsBiologyProtein Serine-Threonine Kinasesself-renewalHistonesAurora KinasesCell Line TumorReportAutophagyAurora Kinase BHumansTP53PhosphorylationRNA Small InterferingMolecular BiologyMitosisCellular SenescenceCyclin-Dependent Kinase Inhibitor p16EtoposideOvarian NeoplasmsEmbryonal Carcinoma Stem CellsCell BiologyG2-M DNA damage checkpointbeta-GalactosidasepluripotencyAntineoplastic Agents PhytogenicChromatinUp-RegulationG2 Phase Cell Cycle CheckpointsCheckpoint Kinase 2Cancer researchDNA damageFemaleRNA InterferenceRad51 RecombinaseTumor Suppressor Protein p53Cell agingOctamer Transcription Factor-3Developmental BiologyCell cycle (Georgetown, Tex.)
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Gold(I) Biscarbene Complexes Derived from Vascular-Disrupting Combretastatin A-4 Address Different Targets and Show Antimetastatic Potential

2014

Gold N-heterocyclic carbene (NHC) complexes are an emerging class of anticancer drugs. We present a series of gold(I) biscarbene complexes with NHC ligands derived from the plant metabolite combretastatin A-4 (CA-4) that retain its vascular-disrupting effect, yet address different cellular and protein targets. Unlike CA-4, these complexes did not interfere with tubulin, but with the actin cytoskeleton of endothelial and cancer cells. For the highly metastatic 518A2 melanoma cell line this effect was accompanied by a marked accumulation of cells in the G1 phase of the cell cycle and a suppression of active prometastatic matrix metalloproteinase-2. Despite these mechanistic differences the co…

StereochemistryNeovascularization PhysiologicAntineoplastic AgentsBiologyBiochemistryMicechemistry.chemical_compoundCoordination ComplexesTubulinCell Line TumorBibenzylsDrug DiscoveryHuman Umbilical Vein Endothelial CellsAnimalsHumansGeneral Pharmacology Toxicology and PharmaceuticsMelanomaCell ProliferationPharmacologyCombretastatin A-4Tube formationCombretastatinMice Inbred BALB COrganic ChemistryCell cycleActin cytoskeletonG2 Phase Cell Cycle CheckpointsActin CytoskeletonChorioallantoic membranechemistryDrug Resistance NeoplasmCell cultureCancer cellMCF-7 CellsCancer researchMolecular MedicineGoldHT29 CellsMethaneChemMedChem
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Synthesis of Combretastatin A-4 and 3′-Aminocombretastatin A-4 derivatives with Aminoacid Containing Pendants and Study of their Interaction with Tub…

2020

Natural product combretastatin A-4 (CA-4) and its nitrogenated analogue 3&prime

Vascular Endothelial Growth Factor ACell cycle checkpoint<i>htert</i>Pharmaceutical ScienceApoptosisAnalytical Chemistrychemistry.chemical_compound0302 clinical medicineDrug DiscoveryStilbenesc-<i>myc</i>Telomerase0303 health sciences<i>vegf</i>biologyNeovascularization PathologicChemistry3′-aminocombretastatin a-4Cell cycle<i>c-Myc</i>VEGFc-MycBiochemistryChemistry (miscellaneous)030220 oncology & carcinogenesisMCF-7 CellsMolecular Medicinecytotoxicitycell cyclehTERTHT29 CellsArticleProto-Oncogene Proteins c-mycmicrotubuleslcsh:QD241-44103 medical and health sciencesStructure-Activity Relationshiplcsh:Organic chemistryMicrotubuleCell Line TumorHumansPhysical and Theoretical Chemistry030304 developmental biologyCell ProliferationCombretastatinCombretastatin A-4Cell growthOrganic ChemistryAntineoplastic Agents PhytogenicTubulintubulinCell cultureA549 Cellsbiology.proteinM Phase Cell Cycle Checkpointscombretastatin a-4Drug Screening Assays AntitumorMolecules
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Wee1 inhibition potentiates Wip1-dependent p53-negative tumor cell death during chemotherapy

2016

AbstractInactivation of p53 found in more than half of human cancers is often associated with increased tumor resistance to anti-cancer therapy. We have previously shown that overexpression of the phosphatase Wip1 in p53-negative tumors sensitizes them to chemotherapeutic agents, while protecting normal tissues from the side effects of anti-cancer treatment. In this study, we decided to search for kinases that prevent Wip1-mediated sensitization of cancer cells, thereby interfering with efficacy of genotoxic anti-cancer drugs. To this end, we performed a flow cytometry-based screening in order to identify kinases that regulated the levels of γH2AX, which were used as readout. Another criter…

Wip1ApoptosisCell Cycle ProteinsPharmacologyMESH: G2 Phase Cell Cycle CheckpointsHistonesMESH : PhosphorylationMiceMESH : Cell Cycle ProteinsMESH: AnimalsMESH: Tumor Suppressor Protein p53MESH: HistonesKinaseTp53 mutationsMESH : Mice Transgenic3. Good healthProtein Phosphatase 2CSurvival RateMESH : Antineoplastic AgentsH2ax phosphorylationP53 activationMESH: Protein Phosphatase 2CRNA InterferenceMESH : Colorectal NeoplasmsMESH : Carrier ProteinsHistone H2axMESH: MitochondriaImmunologyHuman fibroblastsMESH: Carrier ProteinsAntineoplastic AgentsMESH: Protein-Tyrosine KinasesMESH: Protein-Serine-Threonine KinasesMESH : Cisplatin03 medical and health sciencesMESH: Cell Cycle ProteinsGenotoxic stressMESH : Protein-Tyrosine KinasesHumansMESH : HistonesAnticancer TherapyMESH: DNA DamageCisplatinMESH: HumansMESH: Phosphorylation[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyMESH : HumansMESH : Nuclear Proteins030104 developmental biologyCancer cellMESH: Antineoplastic AgentsCisplatinCarrier ProteinsMESH: Nuclear ProteinsMESH : ApoptosisDna-damage response0301 basic medicineCancer ResearchMESH: Caspase 3MESH : Caspase 3PhosphorylationCytotoxicityMESH : DNA DamageSensitizationmedicine.diagnostic_testCaspase 3Nuclear ProteinsProtein-Tyrosine KinasesMESH : Survival RateMitochondriaG2 Phase Cell Cycle CheckpointsWee1medicine.anatomical_structureMESH : Protein Phosphatase 2COriginal ArticleMESH : MitochondriaColorectal Neoplasmsmedicine.drugMESH : Protein-Serine-Threonine KinasesMESH: Cell Line TumorMESH: Survival RateMESH: Mice TransgenicMESH: RNA InterferencePhosphataseMice Transgenic[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyProtein Serine-Threonine KinasesFlow cytometryCellular and Molecular NeuroscienceCell Line TumorMESH : MicemedicineAnimalsMESH: MiceMESH : Cell Line TumorMESH: ApoptosisCell BiologyMESH : Tumor Suppressor Protein p53MESH: CisplatinCancer researchbiology.proteinMESH : AnimalsMESH : G2 Phase Cell Cycle CheckpointsMESH : RNA InterferenceTumor Suppressor Protein p53MESH: Colorectal NeoplasmsDNA DamageCell Death & Disease
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Depletion ofL-arginine induces autophagy as a cytoprotective response to endoplasmic reticulum stress in human T lymphocytes

2012

PMCID: PMC3494587

X-Box Binding Protein 1Proteasome Endopeptidase ComplexProgrammed cell deathXBP1CD3 ComplexMAP Kinase Signaling SystemRNA SplicingT-LymphocytesT cellDown-RegulationApoptosisRegulatory Factor X Transcription FactorsUbiquitin-Activating EnzymesProtein Serine-Threonine KinasesBiologyArginineLymphocyte ActivationAutophagy-Related Protein 7Jurkat cellsJurkat CellsEndoribonucleasesAutophagymedicineHumansMolecular BiologyCell ProliferationTOR Serine-Threonine KinasesAutophagyMembrane ProteinsCell BiologyBECN1Endoplasmic Reticulum StressG1 Phase Cell Cycle CheckpointsBasic Research Paper3. Good healthCell biologyDNA-Binding Proteinsmedicine.anatomical_structureCytoprotectionApoptosisUnfolded protein responseBeclin-1MitogensApoptosis Regulatory ProteinsLysosomesProto-Oncogene Proteins c-aktTranscription FactorsAutophagy
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Cytotoxicity and modes of action of three naturally occurring xanthones (8-hydroxycudraxanthone G, morusignin I and cudraxanthone I) against sensitiv…

2014

Abstract Background Resistance of cancer to chemotherapy remains a challenging issue for scientists as well as physicians. Naturally occurring xanthones possess a variety of biological activities such as anti-inflammatory, anti-bacterial, and anti-cancer effects. The present study was aimed at investigating the cytotoxicity and the modes of action of three naturally occurring xanthones namely, morusignin I (1), 8-hydroxycudraxanthone G (2) and cudraxanthone I (3) against a panel of nine cancer cell lines, including various sensitive and drug-resistant phenotypes. Methods The cytotoxicity of the compounds was determined using a resazurin reduction assay, whereas the caspase-Glo assay was use…

XanthonesPharmaceutical ScienceApoptosisCaspase 8Flow cytometryCell Line TumorNeoplasmsDrug DiscoverymedicineHumansCytotoxicityCaspaseMembrane Potential MitochondrialPharmacologybiologymedicine.diagnostic_testPlant ExtractsCancerCell Cycle CheckpointsHep G2 CellsCell cyclemedicine.diseaseAntineoplastic Agents PhytogenicDrug Resistance MultipleComplementary and alternative medicineDrug Resistance NeoplasmApoptosisCell cultureCaspasesImmunologybiology.proteinCancer researchMolecular MedicineGarciniaPhytotherapyPhytomedicine
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