Search results for " Cell Cycle"

showing 10 items of 92 documents

Effects of resveratrol analogs on cell cycle progression, cell cycle associated proteins and 5fluoro-uracil sensitivity in human derived colon cancer…

2009

International audience; Epidemiological studies suggested that trans-resveratrol, a wine grape component, could prevent malignant tumor development. This compound also demonstrated cytostatic and cytotoxic effects on tumor cells in vitro. To obtain trans-resveratrol derivatives with a better cellular uptake and enhanced antiproliferative effects, we synthesized a triacetate derivative as well as an oligomer, epsilon-viniferin and its acetylated form, epsilon-viniferin penta-acetate. We also obtained vineatrol, a wine grape shoot extract that associates several polyphenols that may act synergistically, including trans-resveratrol and epsilon-viniferin. We show here that resveratrol triacetat…

Cancer ResearchCyclin AFluorescent Antibody TechniqueCell Cycle ProteinsMESH: Cell CycleMESH: Flow CytometryMESH : Blotting WesternResveratrolmedicine.disease_causeWine grapeMESH: Drug SynergismImmunoenzyme Techniqueschemistry.chemical_compoundMESH: PhenolsMESH : Cell Cycle ProteinsMESH : Tumor Cells CulturedMESH: StilbenesStilbenesTumor Cells CulturedMESH : Cell ProliferationMESH: Fluorescent Antibody TechniqueMESH: Antimetabolites AntineoplasticbiologyKinaseMESH : Antimetabolites AntineoplasticCell Cyclefood and beveragesDrug SynergismCell cycleFlow CytometryMESH : Colonic NeoplasmsOncologyBiochemistryColonic NeoplasmsMESH : FluorouracilFluorouracilMESH : PhenolsAntimetabolites AntineoplasticMESH : Drug SynergismMESH : Flow CytometryBlotting WesternMESH : ImmunoprecipitationMESH : StilbenesMESH: Cell Cycle ProteinsPhenolsMESH : Immunoenzyme TechniquesMESH: Cell ProliferationMESH : Cell Cycle[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologymedicineHumansImmunoprecipitationMESH: Blotting Western[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: Tumor Cells CulturedKinase activityMESH: Immunoenzyme Techniques[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyBenzofuransCell ProliferationMESH: Colonic NeoplasmsMESH: HumansMESH : BenzofuransMESH: ImmunoprecipitationMESH : HumansMESH: BenzofuransMESH : Fluorescent Antibody TechniquechemistryResveratrolCell culturebiology.proteinCarcinogenesisMESH: Fluorouracil
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The new iodoacetamidobenzofuran derivative TR120 decreases STAT5 expression and induces antitumor effects in imatinib-sensitive and imatinib-resistan…

2013

The identification of novel compounds modulating the expression/activity of molecular targets downstream to BCR-ABL could be a new approach in the treatment of chronic myeloid leukemias (CMLs) resistant to imatinib or other BCR-ABL-targeted molecules. Recently, we synthesized a new class of substituted 2-(3,4,5-trimethoxybenzoyl)-2-N,N-dimethylamino-benzo[b]furans, and among these 3-iodoacetylamino-6-methoxybenzofuran-2-yl(3,5-trimethoxyphenyl)methanone (TR120) showed marked cytotoxic activity in BCR-ABL-expressing cells. Interestingly, TR120 was more potent than imatinib in cell growth inhibition and apoptosis induction in both BCR-ABL-expressing K562 and KCL22 cells. Moreover, it showed a…

Cancer ResearchFusion Proteins bcr-ablApoptosisPiperazinesSettore MED/15 - Malattie Del Sanguechemistry.chemical_compoundhemic and lymphatic diseasesSTAT5 Transcription FactorCytotoxic T cellPharmacology (medical)Cyclin D1STAT5biologyDrug SynergismCell cycleNeoplasm ProteinsGene Expression Regulation NeoplasticLeukemiaOncologyProto-Oncogene Proteins c-bcl-2BenzamidesImatinib MesylateGrowth inhibitionmedicine.drugbcl-X ProteinDown-RegulationAntineoplastic AgentsBone Marrow CellsResting Phase Cell CycleColony-Forming Units AssayBenzophenonesNecrosisCell Line TumorLeukemia Myelogenous Chronic BCR-ABL PositivemedicineHumansneoplasmsBenzofuransPharmacologyG1 PhaseImatinibBCR-ABL chronic myeloid leukemia imatinib resistance STAT5 tyrosine kinase inhibitorsmedicine.diseaseSettore CHIM/08 - Chimica FarmaceuticaGenes bcl-1Genes bcl-2PyrimidineschemistryApoptosisDrug Resistance NeoplasmSettore BIO/14 - FarmacologiaCancer researchbiology.proteinK562 CellsK562 cells
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HIF-1 is involved in the negative regulation of AURKA expression in breast cancer cell lines under hypoxic conditions

2013

Numerous microarray-based gene expression studies performed on several types of solid tumors revealed significant changes in key genes involved in progression and regulation of the cell cycle, including AURKA that is known to be overexpressed in many types of human malignancies. Tumor hypoxia is associated with poor prognosis in several cancer types, including breast cancer (BC). Since hypoxia is a condition that influences the expression of many genes involved in tumorigenesis, proliferation, and cell cycle regulation, we performed a microarray-based gene expression analysis in order to identify differentially expressed genes in BC cell lines exposed to hypoxia. This analysis showed that h…

Cancer ResearchSettore MED/06 - Oncologia MedicaDown-RegulationBreast NeoplasmsBiologymedicine.disease_causeAURKA Breast cancer Cell cycle HIF-1a HypoxiaCell Line TumorGene expressionTranscriptional regulationmedicineHumansPromoter Regions GeneticAurora Kinase ARegulation of gene expressionGene knockdownTumor hypoxiaCell cycleHypoxia (medical)Hypoxia-Inducible Factor 1 alpha SubunitMolecular biologyCell HypoxiaGene Expression Regulation NeoplasticOncologyGene Knockdown TechniquesCancer researchFemalemedicine.symptomCarcinogenesisBreast Cancer Research and Treatment
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Galangin increases the cytotoxic activity of imatinib mesylate in imatinib-sensitive and imatinib-resistant Bcr-Abl expressing leukemia cells

2008

Resistance to imatinib mesylate is an emergent problem in the treatment of Bcr-Abl expressing myelogenous leukemias and additional therapeutic strategies are required. We observed that galangin, a non-toxic, naturally occurring flavonoid was effective as anti-proliferative, and apoptotic agent in Bcr-Abl expressing K562 and KCL22 cells and in imatinib mesylate resistant K562-R and KCL22-R cells. Galangin induced an arrest of cells in G0–G1phase of cell cycle and a decrease in pRb, cdk4, cdk1, cycline B levels; moreover, it was able to induce a monocytic differentiation of leukemic Bcr-Abl+ cells. Of note, galangin caused a decrease in Bcl-2 levels and markedly increased the apoptotic activi…

Cancer ResearchSettore MED/17 - Malattie InfettiveSettore MED/06 - Oncologia MedicaApoptosisPharmacologyResting Phase Cell CyclePiperazineschemistry.chemical_compoundCell Line TumorLeukemia Myelogenous Chronic BCR-ABL Positivehemic and lymphatic diseasesAntineoplastic Combined Chemotherapy ProtocolsmedicineHumansCytotoxic T cellChrysinneoplasmsFlavonoidsLeukemiaG1 PhaseApoptosiCell DifferentiationImatinibmedicine.diseaseSettore CHIM/08 - Chimica FarmaceuticaGalanginLeukemiaPyrimidinesImatinib mesylateOncologychemistryDrug Resistance NeoplasmImatinibBenzamidesSettore BIO/14 - FarmacologiaImatinib MesylateK562 CellsFisetinBcr-AblK562 cellsmedicine.drugCancer Letters
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Inhibitory effects oftrans-resveratrol analogs molecules on the proliferation and the cell cycle progression of human colon tumoral cells

2008

International audience; Resveratrol may function as a cancer chemopreventive agent. However, few data are available on the antitumoral activities of its dimer, epsilon-viniferin, also present in human diet. So, the effects of resveratrol, epsilon-viniferin, of their acetylated forms (resveratrol triacetate, epsilon-viniferin pentaacetate) and of vineatrol (a wine grape extract) were compared on human adenocarcinoma colon cells. Resveratrol and resveratrol triacetate inhibit cell proliferation and arrest cell cycle. epsilon-Viniferin and epsilon-viniferin pentaacetate slightly reduce cell proliferation. Vineatrol inhibits cell proliferation and favors an accumulation in the S phase of the ce…

Cell Membrane Permeabilityendocrine system diseasesvineatrolMESH: Cell CycleMESH: DNA ReplicationMESH: Flow CytometryresveratrolResveratrolMESH : Antineoplastic Agents PhytogenicWine grapechemistry.chemical_compoundMESH: Structure-Activity RelationshipMESH: StilbenesStilbenesMESH : Structure-Activity RelationshipMESH: Cell Membrane Permeabilityskin and connective tissue diseasesfood and beveragesDNA NeoplasmMESH : Cell DivisionCell cycleFlow CytometryMESH : Colonic Neoplasmscolon cancerBiochemistryColonic NeoplasmsMESH: Cell Divisioncell cycleMESH : DNA NeoplasmCell Divisionhormones hormone substitutes and hormone antagonistsMESH : DNA ReplicationBiotechnologyDNA ReplicationMESH: XenobioticsMESH: Cell Line TumorMESH : Flow CytometryMESH: Antineoplastic Agents PhytogenicMESH: DNA NeoplasmMESH : XenobioticsBiologyXenobioticsMESH : StilbenesStructure-Activity RelationshipCell Line TumorMESH : Cell Cycle[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyHumansStructure–activity relationship[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologypolyphenolsS phaseMESH: Colonic NeoplasmsMESH: HumansMESH : Cell Line TumorCell growthorganic chemicalsMESH : HumansAntineoplastic Agents PhytogenicchemistryMESH : Cell Membrane PermeabilityAcetylationCell cultureCancer researchFood ScienceMolecular Nutrition & Food Research
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Synthesis and biological evaluation of a D-ring-contracted analogue of lamellarin D

2017

A D-ring contracted analogue of the strongly cytotoxic marine pyrrole alkaloid lamellarin D was synthesized and investigated for its antiproliferative action towards a wild type and a multidrug resistant (MDR) cancer cell line. The compound was found to inhibit tumor cell growth at submicromolar concentrations and showed a lower relative resistance in the MDR cell line than the antitumor drug camptothecin to which lamellarin D shows cross resistance and with which lamellarin D shares the same binding site.

Cell SurvivalStereochemistryClinical BiochemistryPharmaceutical ScienceAntineoplastic Agents010402 general chemistryHeterocyclic Compounds 4 or More Rings01 natural sciencesBiochemistrychemistry.chemical_compoundCoumarinsCell Line TumorDrug DiscoverymedicineHumansCytotoxic T cellheterocyclic compoundsBinding siteMolecular BiologyBinding Sites010405 organic chemistryChemistryAlkaloidOrganic ChemistryWild typeIsoquinolinesProtein Structure Tertiary0104 chemical sciencesG2 Phase Cell Cycle CheckpointsMolecular Docking SimulationMultiple drug resistanceDNA Topoisomerases Type IDrug Resistance NeoplasmMutagenesisCell cultureLamellarin DM Phase Cell Cycle CheckpointsMolecular MedicineTopoisomerase I InhibitorsCamptothecinmedicine.drugBioorganic & Medicinal Chemistry
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Cisplatin sensitivity is related to late DNA damage processing and checkpoint control rather than to the early DNA damage response

2008

The present study aimed at elucidating mechanisms dictating cell death triggered by cisplatin-induced DNA damage. We show that CL-V5B hamster mutant cells, a derivative of V79B, are hypersensitive to cisplatin-induced apoptotic death. CL-V5B cells are characterized by attenuated cisplatin-induced early (2-6 h) stress response, such as phosphorylation of stress-activated protein kinases (SAPK/JNK), ATM and Rad3-related (ATR) protein kinase, histone H2AX and checkpoint kinase-1 (Chk-1). Human FANCC cells also showed a reduced phosphorylation of H2AX and SAPK/JNK at early time point after cisplatin treatment. This was not the case for BRCA2-defective VC-8 hamster cells, indicating that the FA …

Cell cycle checkpointCisplatin-DNA adducts ; DNA repair ; Interstrand cross links ; DNA damage response ; Cell cycle checkpoint ; Cell deathDNA damageDNA repairHealth Toxicology and MutagenesisApoptosisCell LineHistonesDNA AdductsCricetinaeGeneticsmedicineAnimalsHumansCHEK1PhosphorylationMolecular BiologyChromosome AberrationsCisplatinbiologyJNK Mitogen-Activated Protein KinasesDNA replicationG2-M DNA damage checkpointMolecular biologyCell biologyHistonebiology.proteinCisplatinDNA DamageMutagensmedicine.drug
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Pyrazole[3,4-d]pyrimidine derivatives loaded into halloysite as potential CDK inhibitors

2021

Uncontrolled cell proliferation is a hallmark of cancer as a result of rapid and deregulated progression through the cell cycle. The inhibition of cyclin-dependent kinases (CDKs) activities is a promising therapeutic strategy to block cell cycle of tumor cells. In this work we reported a new example of nanocomposites based on halloysite nanotubes (HNTs)/pyrazolo[3,4-d]pyrimidine derivatives (Si306 and Si113) as anticancer agents and CDK inhibitors. HNTs/Si306 and HNTs/Si113 nanocomposites were synthesized and characterized. The release kinetics were also investigated. Antitumoral activity was evaluated on three cancer cell lines (HeLa, MDA-MB-231 and HCT116) and the effects on cell cycle ar…

Cell cycle checkpointPyrimidinePharmaceutical Science02 engineering and technologyCDK inhibitors; Halloysite; Nanocomposites; Pyrazolo[34-d]pyrimidine derivatives; Cell Cycle Checkpoints; Cell Line Tumor; Clay; Humans; Pyrazoles; PyrimidinesPyrazolo[34-d]pyrimidine derivativesPyrazole030226 pharmacology & pharmacyCell LineNanocompositesHeLa03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCyclin-dependent kinaseCell Line TumorPyrazolo[3HumansSettore BIO/06 - Anatomia Comparata E CitologiaSettore CHIM/02 - Chimica FisicaTumorbiologyChemistryKinaseCell growth4-d]pyrimidine derivativesHalloysiteSettore CHIM/06 - Chimica OrganicaCell Cycle CheckpointsCell cycle021001 nanoscience & nanotechnologybiology.organism_classificationSettore BIO/18 - GeneticaPyrimidinesSettore CHIM/03 - Chimica Generale E Inorganicabiology.proteinCancer researchClayPyrazoles0210 nano-technologyCDK inhibitors
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Dihydrocucurbitacin B Inhibits Delayed Type Hypersensitivity Reactions by Suppressing Lymphocyte Proliferation

2007

We have studied the effects of dihydrocucurbitacin B, a triterpene isolated from Cayaponia tayuya roots, on different models of delayed type hypersensitivity (DTH) in mice, as well as on T-lymphocyte proliferation and the mediators involved. In experiments with mice, dihydrocucurbitacin B inhibited the inflammatory reactions induced by oxazolone, dinitrofluorobenzene, and sheep red blood cells, reducing both the edema and cell infiltration. Moreover, the analysis of inflamed tissues showed that dihydrocucurbitacin B reduced the presence of the most relevant cytokines implicated in these processes, including interleukin-1 beta, interleukin-4, and tumor necrosis factor-alpha. Dihydrocucurbita…

CellLymphocyte proliferationLymphocyte ActivationResting Phase Cell CycleOxazoloneMicechemistry.chemical_compoundCyclinsmedicineAnimalsHypersensitivity DelayedCyclinInflammationPharmacologyNFATC Transcription FactorsbiologyNFATCell cyclebiology.organism_classificationMolecular biologyTriterpenesCayaponia tayuyaDisease Models Animalmedicine.anatomical_structurechemistryImmunologyCytokinesMolecular MedicineTumor necrosis factor alphaJournal of Pharmacology and Experimental Therapeutics
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Pyrrolo[2',3':3,4]cyclohepta[1,2-d][1,2]oxazoles, a New Class of Antimitotic Agents Active against Multiple Malignant Cell Types

2020

A new class of pyrrolo[2',3':3,4]cyclohepta[1,2-d][1,2]oxazoles was synthesized for the treatment of hyperproliferative pathologies, including neoplasms. The new compounds were screened in the 60 human cancer cell lines of the NCI drug screen and showed potent activity with GI50 values reaching the nanomolar level, with mean graph midpoints of 0.08-0.41 μM. All compounds were further tested on six lymphoma cell lines, and eight showed potent growth inhibitory effects with IC50 values lower than 500 nM. Mechanism of action studies showed the ability of the new [1,2]oxazoles to arrest cells in the G2/M phase in a concentration dependent manner and to induce apoptosis through the mitochondrial…

CellsMitosisAntineoplastic AgentsApoptosisAntimitotic AgentsDrug Screening Assays[12]oxazoles antimitotic agents lymphoma tubulin polymerization inhibitorsDose-Response RelationshipStructure-Activity Relationshipchemistry.chemical_compoundModelsDrug DiscoverymedicineHumansStructure–activity relationshipColchicineOxazolesAntimitotic Agents; Antineoplastic Agents; Apoptosis; Cell Proliferation; Cells Cultured; Dose-Response Relationship Drug; Drug Screening Assays Antitumor; G2 Phase Cell Cycle Checkpoints; HeLa Cells; Humans; Mitosis; Models Molecular; Molecular Structure; Oxazoles; Structure-Activity RelationshipCell Proliferationchemistry.chemical_classificationReactive oxygen speciesCulturedMolecular StructureChemistryMolecularDepolarizationAntitumorMolecular biologyG2 Phase Cell Cycle CheckpointsMechanism of actionApoptosisCell cultureMolecular MedicineAntimitotic AgentDrugmedicine.symptomHeLa Cells
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