Search results for "G1 phase"

showing 10 items of 36 documents

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
researchProduct

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
researchProduct

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
researchProduct

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
researchProduct

Differential gene expression in p53-mediated G(1) arrest of human fibroblasts after gamma-irradiation or N-phosphoacetyl-L-aspartate treatment.

2000

In human fibroblasts, N:-phosphoacetyl-L-aspartate (PALA) and gamma-radiation induce reversible and irreversible p53-mediated G(1) cell cycle arrest, respectively. By coupling the premature chromosome condensation technique to fluorescence in situ hybridization, we found no evidence of DNA damage after PALA treatment. We used representational difference analysis (cDNA-RDA) to study changes in gene expression after PALA treatment and gamma-radiation in normal human fibroblasts. The mammary-derived growth inhibitor (MDGI) gene was expressed in PALA-treated cells. Ectopic MDGI expression arrested PALA-treated but not irradiated RKO cells. Expression of an antisense RNA against MDGI resulted in…

Phosphonoacetic AcidCancer ResearchTumor suppressor geneIn situ hybridizationBiologyFatty Acid-Binding ProteinsCell LineGene expressionHumansGeneIn Situ Hybridization FluorescenceMetaphaseSkinExpressed Sequence TagsExpressed sequence tagAspartic AcidCell CycleG1 PhaseChromosome MappingG0 phaseGeneral MedicineCell cycleFibroblastsMolecular biologyGrowth InhibitorsGene Expression RegulationGamma RaysKaryotypingRepresentational difference analysisTumor Suppressor Protein p53Carrier ProteinsCell Adhesion MoleculesFatty Acid Binding Protein 3Chromosomes Human Pair 7Carcinogenesis
researchProduct

Synthesis and induction of G0–G1 phase arrest with apoptosis of 3,5-dimethyl-6-phenyl-8-(trifluoromethyl)-5,6-dihydropyrazolo[3,4-f][1,2,3,5]tetrazep…

2007

The multistep synthesis of 3,5-dimethyl-6-phenyl-8-(trifluoromethyl)-5,6-dihydropyrazolo[3,4-f][1,2,3,5]tetrazepin-4(3H)-one 15 has been carried out. The compound showed antiproliferative and apoptotic effects against K562, K562-R (imatinib mesilate resistant), HL60 and multidrug resistant (MDR) HL60 cell lines. Compound 15 showed a pro-apoptotic activity against HL60 and K562 resistant cell lines markedly higher than etoposide and busulfan, respectively. Flow cytometry studies carried out on K562 cells allowed to establish that 15 induces G0-G1 phase arrest followed by apoptosis.

HL60StereochemistryApoptosisHL-60 CellsAntiproliferative activityResting Phase Cell CycleChemical synthesisPyrazolo[34-f][1234]tetrazepinoneFlow cytometrychemistry.chemical_compoundhemic and lymphatic diseasesDrug DiscoverymedicineHumansCytotoxicityEtoposideG0-G1 arrestPharmacologyTrifluoromethylMolecular Structuremedicine.diagnostic_testOrganic ChemistryG1 PhaseApoptosiAzepinesGeneral MedicineSettore CHIM/08 - Chimica FarmaceuticaMolecular biologyMultiple drug resistancechemistryApoptosisDrug resistancePyrazoles1234-TetrazepinoneK562 Cellsmedicine.drugEuropean Journal of Medicinal Chemistry
researchProduct

Identification of a Terphenyl Derivative that Blocks the Cell Cycle in the G0−G1 Phase and Induces Differentiation in Leukemia Cells

2006

To further explore the SAR of resveratrol-related trans-stilbene derivatives, here we describe the synthesis of (a) a series of 3,5-dimethoxy analogues in which a variety of substituents were introduced at positions 2', 3', 4', and 5' of the stilbene scaffold and (b) a second group of derivatives (2-phenylnaphthalenes and terphenyls) that incorporate a phenyl ring as a bioisosteric replacement of the stilbene alkenyl bridge. We thoroughly characterized all of the new compounds with respect to their apoptosis-inducing activity and their effects on the cell cycle. One of the new derivatives, 13g, behaved differently from the others, as it was able to block the cell cycle in the G(0)-G(1) phas…

StereochemistryCellular differentiationFusion Proteins bcr-ablAntineoplastic AgentsApoptosis.ResveratrolResting Phase Cell CycleChemical synthesisStructure-Activity Relationshipchemistry.chemical_compoundLeukemia Promyelocytic AcuteCell Line TumorTerphenyl CompoundsTerphenylStilbenesDrug DiscoveryHumansStructure–activity relationshipATP Binding Cassette Transporter Subfamily B Member 1G1 PhaseCell DifferentiationCell cycleIn vitrochemistryDrug Resistance NeoplasmResveratrolCell cultureMolecular MedicineDrug Screening Assays AntitumorJournal of Medicinal Chemistry
researchProduct

AMG900 as novel inhibitor of the translationally controlled tumor protein

2020

Abstract Introduction Cancer is one of the leading causes of death worldwide. Classical cytotoxic chemotherapy exerts high side effects and low tumor selectivity. Translationally controlled tumor protein (TCTP) is a target for differentiation therapy, a promising, new therapeutic approach, which is expected to be more selective and less toxic than cytotoxic chemotherapy. The aim of the present investigation was to identify novel TCTP inhibitors. Methods We performed in silico screening and molecular docking using a chemical library of more than 31,000 compounds to identify a novel inhibitor of TCTP. We tested AMG900 in vitro for binding to TCTP by microscale thermophoresis and co-immunoprec…

0301 basic medicineApoptosisCell Cycle ProteinsToxicologyResting Phase Cell CycleFlow cytometry03 medical and health sciences0302 clinical medicineCyclin D1Differentiation therapyCell Line TumorNeoplasmsTranslationally-controlled tumor proteinBiomarkers TumormedicineHumansCyclin D3medicine.diagnostic_testbiologyChemistryG1 PhaseTumor Protein Translationally-Controlled 1General MedicineMolecular Docking SimulationBlot030104 developmental biologyProtein Biosynthesis030220 oncology & carcinogenesisCancer cellMCF-7 CellsCancer researchbiology.proteinPhthalazinesCyclin-dependent kinase 6Chemico-Biological Interactions
researchProduct

Cytotoxic Activity of Organotin(IV) Derivatives with Triazolopyrimidine Containing Exocyclic Oxygen Atoms

2020

In this study cytotoxicity of organotin(IV) compounds with 1,2,4-triazolo[1,5-a]pyrimidines, Me3Sn(5tpO) (1), n-Bu3Sn(5tpO) (2), Me3Sn(mtpO) (3), n-Bu3Sn(mtpO) (4), n-Bu3Sn(HtpO2) (5), Ph3Sn(HtpO2) (6) where 5HtpO = 4,5-dihydro-5-oxo-[1,2,4]triazolo-[1,5-a]pyrimidine, HmtpO = 4,7-dihydro-5-methyl-7-oxo-[1,2,4]triazolo-[1,5-a]pyrimidine, and H2tpO2 = 4,5,6,7-tetrahydro-5,7- dioxo-[1,2,4]triazolo-[1,5-a]-pyrimidine, was assessed on three different human tumor cell lines: HCT-116 (colorectal carcinoma), HepG2 (hepatocarcinoma) and MCF-7 (breast cancer). While 1 and 3 were inactive, compounds 2, 4, 5 and 6 inhibited the growth of the three tumor cell lines with IC50 values in the submicromolar …

DenticityCellPharmaceutical Science01 natural sciencesAnalytical Chemistrychemistry.chemical_compoundDrug DiscoveryOrganotin CompoundstriazolopyrimidineCytotoxicityMembrane Potential MitochondrialCytotoxinsapoptosisBiological activityHep G2 CellsG2 Phase Cell Cycle CheckpointsGene Expression Regulation Neoplasticmedicine.anatomical_structureChemistry (miscellaneous)Mitochondrial MembranesMCF-7 CellsMolecular MedicineCyclin-Dependent Kinase Inhibitor p21crystal structurein vitro anticancer activityPyrimidineCell SurvivalStereochemistryorganotin(iv)010402 general chemistryArticlelcsh:QD241-441Inhibitory Concentration 50Structure-Activity Relationshiplcsh:Organic chemistrymedicineHumansPhysical and Theoretical ChemistryMetallodrug010405 organic chemistryLigandOrganic ChemistryTriazolesHCT116 CellsapoptosiG1 Phase Cell Cycle Checkpoints0104 chemical sciencesPyrimidineschemistrymetallodrugsCell cultureApoptosisDrug DesignTumor Suppressor Protein p53Reactive Oxygen SpeciesMolecules
researchProduct

A sequence element downstream of the yeast HTB1 gene contributes to mRNA 3' processing and cell cycle regulation.

2002

Histone mRNAs accumulate in the S phase and are rapidly degraded as cells progress into the G(2) phase of the cell cycle. In Saccharomyces cerevisiae, fusion of the 3' untranslated region and downstream sequences of the yeast histone gene HTB1 to a neomycin phosphotransferase open reading frame is sufficient to confer cell cycle regulation on the resulting chimera gene (neo-HTB1). We have identified a sequence element, designated the distal downstream element (DDE), that influences both the 3'-end cleavage site selection and the cell cycle regulation of the neo-HTB1 mRNA. Mutations in the DDE, which is located approximately 110 nucleotides downstream of the HTB1 gene, lead to a delay in the…

Untranslated regionSaccharomyces cerevisiae ProteinsGenes FungalMolecular Sequence DataSaccharomyces cerevisiaeGene ExpressionSaccharomyces cerevisiaeRegulatory Sequences Nucleic AcidPrimary transcriptHistonesOpen Reading FramesGene Expression Regulation FungalMolecular BiologyGeneS phaseBase SequencebiologyCell CycleSingle-Strand Specific DNA and RNA EndonucleasesCell BiologyCell cyclebiology.organism_classificationMolecular biologyDNA-Binding ProteinsHistoneMutagenesis Site-Directedbiology.proteinNucleic Acid ConformationRNA 3' End ProcessingG1 phase
researchProduct