Search results for "CDK inhibitor"

showing 6 items of 6 documents

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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The aryl hydrocarbon receptor-dependent deregulation of cell cycle control induced by polycyclic aromatic hydrocarbons in rat liver epithelial cells

2006

Disruption of cell proliferation control by polycyclic aromatic hydrocarbons (PAHs) may contribute to their carcinogenicity. We investigated role of the aryl hydrocarbon receptor (AhR) in disruption of contact inhibition in rat liver epithelial WB-F344 'stem-like' cells, induced by the weakly mutagenic benz[a]anthracene (BaA), benzo[b]fluoranthene (BbF) and by the strongly mutagenic benzo[a]pyrene (BaP). There were significant differences between the effects of BaA and BbF, and those of the strongly genotoxic BaP. Both BaA and BbF increased percentage of cells entering S-phase and cell numbers, associated with an increased expression of Cyclin A and Cyclin A/cdk2 complex activity. Their eff…

Health Toxicology and MutagenesisCyclin AGene ExpressionApoptosisCell Cycle ProteinsCyclin ACell LineBenz(a)AnthracenesBenzo(a)pyreneCytochrome P-450 CYP1A1polycyclic compoundsGeneticsAnimalsRat liver ‘stem-like’ cellsRNA MessengerPolycyclic Aromatic HydrocarbonsRNA Small InterferingMolecular BiologyAryl hydrocarbon receptorCell proliferationCarcinogenCell ProliferationFluorenesBase SequencebiologyChemistryCell growthCell CycleCyclin-Dependent Kinase 2Contact inhibitionEpithelial CellsTransfectionAryl hydrocarbon receptorMolecular biologyPolycyclic aromatic hydrocarbonsPolycyclic Hydrocarbons AromaticRatsReceptors Aryl HydrocarbonBiochemistryApoptosisMultiprotein ComplexesContact inhibitionMutationHepatocytesbiology.proteinCDK inhibitorMutagensMutation Research/Fundamental and Molecular Mechanisms of Mutagenesis
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Suppressor activity of anergic T cells induced by IL-10-treated human dendritic cells: association with IL-2- and CTLA-4-dependent G1 arrest of the c…

2003

We have previously shown that human IL-10-treated dendritic cells (DC) induce an antigen-specific anergy in CD4+ T lymphocytes. These anergic T cells are characterized by an inhibited proliferation, a reduced production of IL-2, and additionally display antigen-specific suppressor activity. In this study we investigated the mechanisms underlying the anergic state and regulatory function of these T cells. We did not observe enhanced rates of programmed cell death of anergic CD4+ suppressor T cells compared to T cells stimulated with mature DC. Cell cycle analysis by DNA staining and Western blot experiments revealed an arrest of anergic CD4+ T suppressor cells in the G1 phase. High levels of…

ImmunoconjugatesRegulatory T cellT-LymphocytesImmunologyApoptosisCell Cycle ProteinsAbataceptCyclin-dependent kinaseAntigens CDmedicineImmunology and AllergyHumansCTLA-4 AntigenIL-2 receptorClonal AnergybiologyTumor Suppressor ProteinsRetinoblastoma proteinDendritic cellDendritic CellsCell cycleAntigens DifferentiationCell biologyInterleukin-10Interleukin 10medicine.anatomical_structurebiology.proteinInterleukin-2CDK inhibitorCell DivisionCyclin-Dependent Kinase Inhibitor p27European journal of immunology
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FUSED NITROGEN HETEROCYCLES AS PROMISING SMALL MOLECULES FOR THE TREATMENT OF CANCER

2020

Photodynamic therapy photosensitizing nitrogen heterocycles CDK inhibitors antiproliferative activitySettore CHIM/08 - Chimica Farmaceutica
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TORC1 coordinates the conversion of Sic1 from a target to an inhibitor of cyclin-CDK-Cks1

2017

Eukaryotic cell cycle progression through G(1)-S is driven by hormonal and growth-related signals that are transmitted by the target of rapamycin complex 1 (TORC1) pathway. In yeast, inactivation of TORC1 restricts G(1)-S transition due to the rapid clearance of G(1) cyclins (Cln) and the stabilization of the B-type cyclin (Clb) cyclin-dependent kinase (CDK) inhibitor Sic1. The latter mechanism remains mysterious but requires the phosphorylation of Sic1-Thr(173) by Mpk1 and inactivation of the Sic1-pThr(173)-targeting phosphatase (PP2A(Cdc55)) through greatwall kinase-activated endosulfines. Here we show that the Sic1-pThr(173) residue serves as a specific docking site for the CDK phospho-a…

BioquímicaBiologiaCDK inhibitor (CDKI)Rim15Sic1cyclin-dependent protein kinase (CDK)G1 cell cycle arrestgreatwall kinase pathwayG(1) cell cycle arrestCks1Articletarget of rapamycin complex 1 (TORC1)Cell Discovery
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Interleukin-2 and its Receptors in Human Solid Tumours: Immunobiology and Clinical Significance

2006

Human carcinomas were found to express IL-2 R and to produce, but not to secrete, IL-2. Intermediate affinity IL-2Rβγ detected on the surface and in the cytoplasm of carcinoma cells binds exogenous IL-2 at the nanomolar or micromolar concentrations and mediates cell cycle arrest (CCA) possibly through the upregulation of the CDK inhibitor p27kipl expression. In contrast, IL-2Rα is modestly expressed on the cell surface, and it may be involved in the intracrine pathway of delivering endogenous IL-2 to the cell surface. IL-2 is a growth factor for human carcinomas, and as it binds to the high-affinity IL-2R, it promotes cellular proliferation by suppressing expression of p27kipl. It also prot…

Interleukin 2IntracrineCell growthChemistryGrowth factormedicine.medical_treatmentCellCell biologymedicine.anatomical_structureDownregulation and upregulationmedicineReceptorCDK inhibitormedicine.drug
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