Search results for "Cell cycle checkpoint"

showing 10 items of 126 documents

Artesunate Impairs Growth in Cisplatin-Resistant Bladder Cancer Cells by Cell Cycle Arrest, Apoptosis and Autophagy Induction

2020

Cisplatin, which induces DNA damage, is standard chemotherapy for advanced bladder cancer (BCa). However, efficacy is limited due to resistance development. Since artesunate (ART), a derivative of artemisinin originating from Traditional Chinese Medicine, has been shown to exhibit anti-tumor activity, and to inhibit DNA damage repair, the impact of artesunate on cisplatin-resistant BCa was evaluated. Cisplatin-sensitive (parental) and cisplatin-resistant BCa cells, RT4, RT112, T24, and TCCSup, were treated with ART (1&ndash

0301 basic medicineautophagyRMCell cycle checkpointDNA RepairDNA damageArtesunateCell Cycle ProteinsArticlegrowth inhibition03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCell Line TumormedicineHumansddc:610Medicine Chinese Traditionalskin and connective tissue diseaseslcsh:QH301-705.5Cell ProliferationCisplatinartesunate (ART)Cell growthAutophagyapoptosisGeneral MedicineCell cycleG1 Phase Cell Cycle Checkpoints030104 developmental biologychemistrylcsh:Biology (General)Urinary Bladder NeoplasmsApoptosisDrug Resistance Neoplasm030220 oncology & carcinogenesisCancer researchbladder cancer (BCa)Growth inhibitioncisplatin resistanceMicrotubule-Associated Proteinsmedicine.drug
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Prospecting for cytotoxic and antiprotozoal 4-aryl-4H-chromenes and 10-aryldihydropyrano[2,3-f]chromenes.

2018

Different studies reported that genetic predisposition or metabolic dysfunction are the risk factors for cancer. Infectious parasitic diseases were listed among factors that predispose to cancer. Because of the resemblance between the life cycle of cancer cells and some parasites, this study aimed to prepare pyran derivatives with cytotoxic and antiprotozoal potencies. Therefore, 7 chromenes, 10 pyranocoumarins, and an unexpected intermediate were obtained from a multi-reagent one-pot reaction. These compounds were evaluated for their cytotoxicity on sensitive and resistant leukemia cancer cells lines and against two protozoan parasites, namely Trypanosoma cruzi and Leishmania amazonensis a…

0301 basic medicinemedicine.drug_classAntiparasiticTHP-1 CellsTrypanosoma cruziAntiprotozoal AgentsPharmaceutical ScienceAntineoplastic AgentsApoptosisPharmacology03 medical and health sciencesStructure-Activity RelationshipParasitic Sensitivity TestsDrug DiscoverymedicineTumor Cells CulturedCytotoxic T cellHumansBenzopyransTrypanosoma cruziCytotoxicityAmastigoteCell ProliferationLeishmaniabiologyDose-Response Relationship DrugMolecular StructureChemistryCancerCell Cycle Checkpointsbiology.organism_classificationmedicine.disease030104 developmental biologyCancer cellAntiprotozoalDrug Screening Assays AntitumorArchiv der Pharmazie
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Synthesis, antiproliferative activity and possible mechanism of action of novel 2-acetamidobenzamides bearing the 2-phenoxy functionality.

2015

Several new 2-(2-phenoxyacetamido)benzamides 17a-v, 21 and 22 were synthesized by stirring in pyridine the acid chlorides 16a-e and the appropriate5-R-4-R1-2-aminobenzamide 15a-e and initially evaluated in vitro for antiproliferative activity against the K562 (human chronic myelogenous leukemia) cell line. Some of synthesized compounds were evaluated for their in vitro antiproliferative activity against the full NCI tumor cell line panel derived from nine clinically isolated cancer types (leukemia, non-small cell lung, colon, CNS, melanoma, ovarian, renal, prostate and breast). The most active compounds caused an arrest of K562 cells in the G0-G1 phase of cell cycle and induction of apoptos…

3003Clinical BiochemistryCellPharmaceutical ScienceAntineoplastic AgentsApoptosisAntiproliferative activityPharmacologyG0/G1 arrestBiochemistryArticle2-(2-Phenoxyacetamido)benzamideAntineoplastic AgentStructure-Activity RelationshipBenzamideSettore BIO/10 - BiochimicaCell Line TumorDrug DiscoveryG1 Phase Cell Cycle CheckpointK562 CellmedicineHumansMolecular BiologyCell ProliferationCell growthChemistryDrug Discovery3003 Pharmaceutical ScienceOrganic ChemistryApoptosiCell cyclemedicine.diseaseCaspaseSettore CHIM/08 - Chimica FarmaceuticaG1 Phase Cell Cycle CheckpointsLeukemiamedicine.anatomical_structureMicroscopy FluorescenceCell cultureApoptosisCaspasesBenzamidesMolecular MedicineDrug Screening Assays AntitumorK562 CellsPro-caspase 3HumanK562 cellsChronic myelogenous leukemiaBioorganicmedicinal chemistry
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Knockdown of NANOG Reduces Cell Proliferation and Induces G0/G1 Cell Cycle Arrest in Human Adipose Stem Cells

2019

The core components of regenerative medicine are stem cells with high self-renewal and tissue regeneration potentials. Adult stem cells can be obtained from many organs and tissues. NANOG, SOX2 and OCT4 represent the core regulatory network that suppresses differentiation-associated genes, maintaining the pluripotency of mesenchymal stem cells. The roles of NANOG in maintaining self-renewal and undifferentiated status of adult stem cells are still not perfectly established. In this study we define the effects of downregulation of NANOG in maintaining self-renewal and undifferentiated state in mesenchymal stem cells (MSCs) derived from subcutaneous adipose tissue (hASCs). hASCs were expanded…

AdultHomeobox protein NANOGDown-RegulationBiologyArticleCatalysisSettore MED/13 - Endocrinologialcsh:ChemistryInorganic ChemistrySOX2human adipose stem cellHumansCell Self RenewalPhysical and Theoretical Chemistrylcsh:QH301-705.5Molecular BiologyCells CulturedSpectroscopyCell Proliferationmolecular_biologyCell growthOrganic ChemistryMesenchymal stem cellDNMT1lentiviral transductionCell DifferentiationMesenchymal Stem CellsNanog Homeobox ProteinGeneral MedicineMiddle AgedCell cycleG1 Phase Cell Cycle CheckpointsComputer Science ApplicationsCell biologySettore MED/18 - Chirurgia GeneraleNANOGlcsh:Biology (General)lcsh:QD1-999Gene Knockdown Techniquesembryonic structures<i>NANOG</i>Female<i>DNMT1</i>CDKN1Bbiological phenomena cell phenomena and immunityStem cellcell cycle regulationAdult stem cell
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Toward a Rational Design of Polyamine-Based Zinc-Chelating Agents for Cancer Therapies.

2020

In vitro viability assays against a representative panel of human cancer cell lines revealed that polyamines L1a and L5a displayed remarkable activity with IC50 values in the micromolar range. Preliminary research indicated that both compounds promoted G1 cell cycle arrest followed by cellular senescence and apoptosis. The induction of apoptotic cell death involved loss of mitochondrial outer membrane permeability and activation of caspases 3/7. Interestingly, L1a and L5a failed to activate cellular DNA damage response. The high intracellular zinc-chelating capacity of both compounds, deduced from the metal-specific Zinquin assay and ZnL2+ stability constant values in solution, strongly sup…

Antineoplastic AgentsApoptosis01 natural sciences03 medical and health scienceschemistry.chemical_compoundStructure-Activity RelationshipCell Line TumorDrug DiscoveryPolyaminesHumansCytotoxicityCaspase030304 developmental biologyChelating Agents0303 health sciencesbiologyMolecular StructureChemistryRational designG1 Phase Cell Cycle Checkpoints0104 chemical sciencesCell biology010404 medicinal & biomolecular chemistryZincModels ChemicalApoptosisCell cultureDrug Designbiology.proteinMolecular MedicineQuantum TheoryDrug Screening Assays AntitumorPolyamineG1 phaseIntracellularJournal of medicinal chemistry
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Dietary polyphenols in chemoprevention and synergistic effect in cancer: Clinical evidences and molecular mechanisms of action

2020

Abstract Background Epidemiological studies has revealed that a diet rich in fruits and vegetables could lower the risk of certain cancers. In this setting, natural polyphenols are potent anticancer bioactive compounds to overcome the non-target specificity, undesirable cytotoxicity and high cost of treatment cancer chemotherapy. Purpose The review focuses on diverse classifications of the chemical diversity of dietary polyphenol and their molecular targets, modes of action, as well as preclinical and clinical applications in cancer prevention. Results The dietary polyphenols exhibit chemo-preventive activity through modulation of apoptosis, autophagy, cell cycle progression, inflammation, …

AntioxidantCell cycle checkpointmedicine.medical_treatmentPharmaceutical ScienceAntineoplastic Agentsmedicine.disease_causeChemopreventionDietary PolyphenolMetastasisNeoplasmsDrug DiscoverymedicineHumansPharmacologyCancer preventionbusiness.industryPolyphenolsfood and beveragesCancermedicine.diseaseDietComplementary and alternative medicinePolyphenolCancer researchMolecular MedicinebusinessCarcinogenesisPhytomedicine
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Involvement of PAR-4 in Cannabinoid-Dependent Sensitization of Osteosarcoma Cells to TRAIL-Induced Apoptosis

2014

The synthetic cannabinoid WIN 55,212-2 is a potent cannabinoid receptor agonist with anticancer potential. Experiments were performed to determine the effects of WIN on proliferation, cell cycle distribution, and programmed cell death in human osteosarcoma MG63 and Saos-2 cells. Results show that WIN induced G2/M cell cycle arrest, which was associated with the induction of the main markers of ER stress (GRP78, CHOP and TRB3). In treated cells we also observed the conversion of the cytosolic form of the autophagosome marker LC3-I into LC3-II (the lipidated form located on the autophagosome membrane) and the enhanced incorporation of monodansylcadaverine and acridine orange, two markers of t…

AutophagosomeautophagyProgrammed cell deathCannabinoids ER stress autophagy TRAIL osteosarcoma cells GRP78/PAR-4 complex.Cannabinoid receptorMorpholinesCellApoptosisTRAILNaphthalenesBiologyGRP78/PAR-4 complex.Applied Microbiology and BiotechnologyTNF-Related Apoptosis-Inducing LigandCadaverineCell Line TumorSettore BIO/10 - BiochimicamedicineHumansRNA Small InterferingEndoplasmic Reticulum Chaperone BiPMolecular BiologyHeat-Shock ProteinsEcology Evolution Behavior and SystematicsCell ProliferationCannabinoid Receptor AgonistsOsteosarcomaCannabinoidsAutophagyCell Cycle Checkpointsosteosarcoma cellsCell BiologyCell cycleEndoplasmic Reticulum StressAcridine OrangeBenzoxazinesCell biologymedicine.anatomical_structureApoptosisAutophagosome membraneApoptosis Regulatory ProteinsER stressMicrotubule-Associated ProteinsResearch PaperDevelopmental Biology
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TORC1 controls G1–S cell cycle transition in yeast via Mpk1 and the greatwall kinase pathway

2015

The target of rapamycin complex 1 (TORC1) pathway couples nutrient, energy and hormonal signals with eukaryotic cell growth and division. In yeast, TORC1 coordinates growth with G1–S cell cycle progression, also coined as START, by favouring the expression of G1 cyclins that activate cyclin-dependent protein kinases (CDKs) and by destabilizing the CDK inhibitor Sic1. Following TORC1 downregulation by rapamycin treatment or nutrient limitation, clearance of G1 cyclins and C-terminal phosphorylation of Sic1 by unknown protein kinases are both required for Sic1 to escape ubiquitin-dependent proteolysis prompted by its flagging via the SCFCdc4 (Skp1/Cul1/F-box protein) ubiquitin ligase complex.…

BioquímicaBiologiaSaccharomyces cerevisiae ProteinsImmunoblottingGeneral Physics and AstronomyCell Cycle ProteinsSaccharomyces cerevisiaeMechanistic Target of Rapamycin Complex 1ArticleGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciences0302 clinical medicineCyclin-dependent kinaseCyclinsImmunoprecipitationProtein Phosphatase 2Cell division control protein 4PhosphorylationProtein kinase ACyclin-Dependent Kinase Inhibitor Proteins030304 developmental biology0303 health sciencesMultidisciplinarybiologyTOR Serine-Threonine KinasesUbiquitin-Protein Ligase ComplexesGeneral ChemistryBlotting NorthernFlow CytometryG1 Phase Cell Cycle CheckpointsSic1Cyclin-Dependent KinasesCell biologyBiochemistryMultiprotein Complexes030220 oncology & carcinogenesisUbiquitin ligase complexbiology.proteinIntercellular Signaling Peptides and ProteinsPhosphorylationTOR Serine-Threonine KinasesMitogen-Activated Protein KinasesPeptidesProtein KinasesCyclin-dependent kinase inhibitor proteinNature Communications
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Preclinical evaluation of antitumor activity of the proteasome inhibitor MLN2238 (ixazomib) in hepatocellular carcinoma cells

2017

AbstractHepatocellular carcinoma (HCC) is one of the common malignancies and is an increasingly important cause of cancer death worldwide. Surgery, chemotherapy, and radiation therapy extend the 5-year survival limit in HCC patients by only 6%. Therefore, there is a need to develop new therapeutic approaches for the treatment of this disease. The orally bioavailable proteasome inhibitor MLN2238 (ixazomib) has been demonstrated to have anticancer activity. In the present study, we investigated the preclinical therapeutic efficacy of MLN2238 in HCC cells through in vitro and in vivo models, and examined its molecular mechanisms of action. MLN2238 inhibited cell viability in human HCC cells He…

Boron Compounds0301 basic medicineCancer ResearchCarcinoma HepatocellularMyeloidCell cycle checkpointImmunologyCellGlycineAntineoplastic AgentsArticleIxazomibAntineoplastic AgentMice03 medical and health sciencesCellular and Molecular Neurosciencechemistry.chemical_compound0302 clinical medicinemedicineAnimalsHumansViability assaylcsh:QH573-671Boron CompoundAnimallcsh:Cytologybusiness.industryLiver NeoplasmsCell Biologydigestive system diseases3. Good health030104 developmental biologymedicine.anatomical_structurechemistryLiver NeoplasmCell cultureApoptosis030220 oncology & carcinogenesisProteasome inhibitorCancer researchbusinessProteasome InhibitorsHumanmedicine.drugCell Death &amp; Disease
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Abstract 1993: Fishing for artemisinin-interacting proteins from human nasopharyngeal cancer cells

2012

Abstract Determining cellular target molecules of drugs by chemical proteomic techniques is complex and tedious. Most approaches rely on activity-based probe profiling and compound-centric chemical proteomics. The antimalarial artemisinin also exerts profound anti-cancer activity, but the mechanisms of action are incompletely understood. In the present study, we have identified artemisinin-interacting target proteins from human nasopharyngeal carcinoma cell line CNE1. Thereby, our approach overcomes usual problems in traditional fishing procedures, because the drug was attached to a polystyrene surface without further chemical modification. Using mass spectrometry we have identified 20 prot…

Cancer ResearchCell cycle checkpointAngiogenesisCell migrationBiologyProteomicsIn vitroCell biologyOncologyBiochemistryNuclear receptormedicineArtemisininMode of actionmedicine.drugCancer Research
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