Search results for "G1 phase"

showing 10 items of 36 documents

As2O3-induced oxidative stress and cycle progression in a human intestinal epithelial cell line (Caco-2)

2007

Foods and drinking water are the main routes for human exposure to inorganic arsenic, the intestinal epithelium being the first barrier against such exogenous toxicants. The present study evaluates the effect of As(III) (0.5-25 microM) upon Caco-2 cells as an intestinal epithelia model. Cell viability, intracellular formation of reactive oxygen species (ROS), mitochondrial membrane potential (Deltapsim) changes, and cell cycle distribution in exposed cultures were evaluated. The intracellular production of ROS was seen to increase in a non-dose dependent manner at all concentrations tested, with impairment of cell mitochondrial enzyme function secondary to a loss of Deltapsim. Concentration…

G2 PhaseCell SurvivalCellTetrazolium SaltsOxidative phosphorylationBiologyToxicologymedicine.disease_causeArsenicalsMembrane PotentialsArsenic TrioxidemedicineHumansViability assaychemistry.chemical_classificationReactive oxygen speciesCell CycleG1 PhaseOxidesGeneral MedicineCell cycleIntestinal epitheliumMitochondriaCell biologyOxidative StressThiazolesmedicine.anatomical_structurechemistryMitochondrial MembranesCaco-2 CellsReactive Oxygen SpeciesOxidative stressIntracellularToxicology in Vitro
researchProduct

Combination of the novel farnesyltransferase inhibitor RPR130401 and the geranylgeranyltransferase-1 inhibitor GGTI-298 disrupts MAP kinase activatio…

1999

To test the Kirsten-Ras (Ki-Ras) alternative prenylation hypothesis in malignant transformation, we used a novel farnesyltransferase inhibitor competitive to farnesyl-pyrophosphate, RPR130401, and a CaaX peptidomimetic geranylgeranyltransferase-1 inhibitor GGTI-298. In Ki-Ras-overexpressing transformed adrenocortical cells, RPR130401 at 1-10 microM inhibited very efficiently the [(3)H]farnesyl but not [(3)H]geranylgeranyl transfer to Ras. However, proliferation of these cells was only slightly sensitive to RPR130401 (IC(50)=30 microM). GGTI-298 inhibited the growth of these cells with an IC(50) of 11 microM but cell lysis was observed at 15 microM. The combination of 10 microM RPR130401 and…

GeranylgeranyltransferaseFarnesyltransferaseSimvastatinIndolesTime FactorsFarnesyltransferaseBiophysicsProtein PrenylationAntineoplastic AgentsKirsten-RasBiochemistryAnti-proliferative effectS PhasePrenylationStructural BiologyAlternative pathwayAdrenal GlandsGeneticsAnimalsFarnesyltranstransferaseLovastatinBinding siteEnzyme InhibitorsMolecular BiologyCells CulturedCell Line TransformedPrenylationAlkyl and Aryl TransferasesbiologyDose-Response Relationship DrugCell growthFarnesyltransferase inhibitorG1 PhaseG1/S transitionDrug SynergismCell BiologyCell cycleFlow CytometryCell biologyRatsGenes rasBiochemistryMitogen-activated protein kinaseBenzamidesbiology.proteinras ProteinsMitogen-Activated Protein KinasesCell DivisionFEBS letters
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

The novel dual PI3K/mTOR inhibitor GDC-0941 synergizes with the MEK inhibitor U0126 in non-small cell lung cancer cells.

2011

Lung cancer is a malignant disease with poor outcome, which has led to a search for new therapeutics. The PI3K/Akt/mTOR and Ras/raf/Erk pathways are key regulators of tumor growth and survival. In the present study, their roles were evaluated by MTT assay, flow cytometry and Western blotting in lung cancer cells. We found that a high efficacy of antitumor activity was shown with GDC-0941 treatment in two gefitinib-resistant non-small cell lung cancer (NSCLC) cell lines, A549 and H460. In addition, H460 cells with activating mutations of PIK3CA were relatively more sensitive to GDC-0941 than A549 cells with wild-type PIK3CA. Furthermore, GDC-0941 was highly efficacious in combination with U0…

MAPK/ERK pathwayCancer ResearchIndazolesLung NeoplasmsApoptosisBiologyBiochemistryPhosphatidylinositol 3-KinasesCarcinoma Non-Small-Cell LungCell Line TumorNitrilesGeneticsmedicineButadienesHumansMolecular BiologyProtein kinase BProtein Kinase InhibitorsPI3K/AKT/mTOR pathwayPhosphoinositide-3 Kinase InhibitorsSulfonamidesOncogeneCell growthMEK inhibitorTOR Serine-Threonine KinasesCancerDrug SynergismCell cyclemedicine.diseaseG1 Phase Cell Cycle Checkpointsrespiratory tract diseasesEnzyme ActivationOncologyCancer researchMolecular MedicineMitogen-Activated Protein KinasesSignal TransductionMolecular medicine reports
researchProduct

Involvement of the transcription factor FoxM1 in contact inhibition

2012

Contact inhibition is a crucial mechanism regulating proliferation in vitro and in vivo. Although it is generally accepted that contact inhibition plays a pivotal role in maintaining tissue homeostasis, the molecular mechanisms of contact inhibition are still not fully understood. FoxM1 is known as a proliferation-associated transcription factor and is upregulated in many cancer types. Vice versa, anti-proliferative signals, such as TGF-β and differentiation signals decrease FoxM1 expression. Here we investigated the role of FoxM1 in contact inhibition in fibroblasts. We show that protein expression of FoxM1 is severely and rapidly downregulated upon contact inhibition, probably by inhibiti…

MAPK/ERK pathwayCyclin ABiophysicsDown-RegulationCell Cycle ProteinsCyclin AProtein Serine-Threonine KinasesBiochemistryMiceDownregulation and upregulationProto-Oncogene ProteinsAnimalsPhosphorylationRNA Small InterferingExtracellular Signal-Regulated MAP KinasesMolecular BiologyTranscription factorTissue homeostasisbiologyContact InhibitionKinaseForkhead Box Protein M1Contact inhibitionForkhead Transcription FactorsCell BiologyG1 Phase Cell Cycle CheckpointsCell biologyNIH 3T3 Cellsbiology.proteinEctopic expressionBiochemical and Biophysical Research Communications
researchProduct

Deregulation of the G1 to S-phase cell cycle checkpoint is involved in the pathogenesis of human osteosarcoma.

2004

Osteosarcoma (OS) displays complex karyotypes with numerical changes as well as structural abnormalities suggesting that several oncogenes and tumor suppressor genes may be implicated in the biology of OS. The aim of our study was to investigate the possible implication of the molecular alterations of the G1 to S-phase checkpoint genes in the pathogenesis of OS. We analyzed samples from 29 patients and found molecular alterations of the RB and TP53 genes in 6 (21%) and 3 (10%) cases, respectively. Homozygous deletion of the INK4A/ARF locus and methylation of INK4A was detected in 3 (10%) and 2 (7%) cases, respectively. CDK4 and MDM2 co-amplification was observed in 1 case (3%). Cyclin D3 is…

MaleCell cycle checkpointAdolescentLocus (genetics)Bone NeoplasmsBiologyPathology and Forensic MedicineS PhasePathogenesisGene duplicationmedicineHumansCHEK1Cyclin D3ChildMolecular BiologyAgedOsteosarcomaReverse Transcriptase Polymerase Chain ReactionCell CycleAge FactorsG1 PhaseGene AmplificationCell BiologyG2-M DNA damage checkpointMiddle Agedmedicine.diseaseGenes cdcHistory 16th CenturyCancer researchOsteosarcomaFemaleChromosomes Human Pair 9Diagnostic molecular pathology : the American journal of surgical pathology, part B
researchProduct

Transcription of the MAT2A gene, coding for methionine adenosyltransferase, is up-regulated by E2F and Sp1 at a chromatin level during proliferation …

2006

Methionine adenosyltransferase (MAT) is an essential enzyme because it catalyzes the formation of S-adenosylmethionine, the main methyl donor. Two MAT-encoding genes (MAT1A, MAT2A) are found in mammals. The latter is expressed in proliferating liver, dedifferentiation and cancer, whereas MAT1A is expressed in adult quiescent hepatocytes. Here, we report studies on the molecular mechanisms controlling the induction of MAT2A in regenerating rat liver and in proliferating hepatocytes. The MAT2A is up-regulated at two discrete moments during liver regeneration, as confirmed by RNApol-ChIP analysis. The first one coincides with hepatocyte priming (i.e. G0-G1 transition), while the second one tak…

MaleChromatin ImmunoprecipitationTranscription GeneticSp1 Transcription FactorMolecular Sequence DataOligonucleotidesElectrophoretic Mobility Shift AssayBiologyBiochemistryS PhaseSequence Homology Nucleic AcidmedicineAnimalsE2F1Electrophoretic mobility shift assayRats WistarPromoter Regions GeneticE2FE2F4Cells CulturedCell ProliferationSp1 transcription factorBase SequenceG1 PhaseMethionine AdenosyltransferaseCell BiologyMolecular biologyChromatinLiver regenerationE2F Transcription FactorsLiver RegenerationRatsUp-Regulationmedicine.anatomical_structureLiverMethionine AdenosyltransferaseHepatocyteHepatocytesProtein BindingThe International Journal of Biochemistry & Cell Biology
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

Three-dimensional structure of the anaphase-promoting complex.

2001

The anaphase-promoting complex (APC) is a cell cycle-regulated ubiquitin-protein ligase, composed of at least 11 subunits, that controls progression through mitosis and G1. Using cryo-electron microscopy and angular reconstitution, we have obtained a three-dimensional model of the human APC at a resolution of 24 A. The APC has a complex asymmetric structure 140 A x 140 A x 135 A in size, in which an outer protein wall surrounds a large inner cavity. We discuss the possibility that this cavity represents a reaction chamber in which ubiquitination reactions take place, analogous to the inner cavities formed by other protein machines such as the 26S proteasome and chaperone complexes. This cag…

Protein subunitUbiquitin-Protein LigasesAnaphase-Promoting Complex-CyclosomeLigasesProtein structureUbiquitinHumansProtein Structure QuaternaryMitosisMolecular Biologychemistry.chemical_classificationDNA ligasebiologyCryoelectron MicroscopyG1 PhaseUbiquitin-Protein Ligase ComplexesCell BiologyPrecipitin TestsCell biologyProtein Structure TertiaryProteasomechemistryChaperone (protein)biology.proteinAnaphase-promoting complexHeLa CellsMolecular cell
researchProduct

Antiproliferative agents that interfere with the cell cycle at the G(1)-->S transition: further development and characterization of a small library o…

2008

In this continuation of our research on derivatives containing the stilbene privileged structure or that are derived from it, we report the results of further studies carried out on the previously initiated collection of compounds. We used a parallel synthetic approach to rapidly obtain small sets of compounds and started the annotation of the library in progress by calculating some physicochemical properties to be eventually correlated with biological activities. A pharmacophore for the antiproliferative activity was also built to summarize the features of the library. We evaluated the antiproliferative and pro-apoptotic activities of all compounds as well as the cell-cycle effects of some…

StereochemistryCellular differentiationAntineoplastic AgentsApoptosisHL-60 CellsBiochemistryS PhaseSmall Molecule Librarieschemistry.chemical_compoundInhibitory Concentration 50Biological profileCell Line TumorDrug DiscoveryStilbenespharmacophoresHumansGeneral Pharmacology Toxicology and PharmaceuticsPhosphorylationPharmacologyChemistryOrganic ChemistryG1 PhaseRetinoblastomaSmall Molecule LibrariesG1/S transitionCell DifferentiationCell cycleFlow CytometryCombinatorial chemistryantitumor agentAntiproliferative AgentsMolecular MedicineTriolcell cyclePharmacophoreC-C couplingK562 Cells
researchProduct