Search results for "kinase inhibitor"

showing 10 items of 414 documents

Mitogenic effects of phospholipase D and phosphatidic acid in transiently permeabilized astrocytes: effects of ethanol.

2003

Investigations of lipid-mediated signalling pathways are often limited by a lack of methods for the intracellular delivery of lipid messengers. We established a procedure for the transient permeabilization of astrocytes by an oxygen-insensitive mutant of streptolysin-O (SLO) to investigate the participation of the phospholipase D (PLD) signalling pathway in astroglial cell proliferation. Exogenous PLD, when incubated in the presence of SLO, caused an increase in DNA synthesis (measured by thymidine incorporation) which was completely suppressed by ethanol (0.3%, v/v). In parallel experiments, phosphatidic acid also induced a dose-dependent mitogenic response which, however, was not affected…

Cell Membrane PermeabilityIndolesmedicine.drug_classPhosphatidic AcidsBiologyBiochemistryDiglyceridesCellular and Molecular Neurosciencechemistry.chemical_compoundBacterial ProteinsmedicinePhospholipase DAnimalsEnzyme InhibitorsProtein kinase ACells CulturedDiacylglycerol kinaseDNA synthesisDose-Response Relationship DrugEthanolPhospholipase DPhosphatidic acidDNAProtein kinase inhibitorRatschemistryBiochemistryAstrocytesStreptolysinslipids (amino acids peptides and proteins)Signal transductionMitogensIntracellularCell DivisionSignal TransductionJournal of neurochemistry
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Recent advances in the development of cyclin-dependent kinase 7 inhibitors.

2019

Abstract Cyclin dependent kinase 7 (CDK7) plays a double role as it activates several other cyclin dependent kinases and participates to the initiation of transcription. This kinase is overexpressed in various types of tumors. Relatively few selective CDK7 inhibitors have been up to now disclosed. Most of these inhibitors belong to two chemical families: pyrazolopyrimidines and pyrazolotriazines on one side and pyrimidines on another side. They also differ by their molecular mechanism of action. Some are acting as competitive inhibitors and some others are covalent inhibitors. With these tools, the understanding of the potential therapeutic interest of CDK7 inhibitors in cancer is rapidly g…

Cell SurvivalAntineoplastic Agents01 natural sciences03 medical and health sciencesDrug DevelopmentCyclin-dependent kinaseTranscription (biology)Cell Line TumorDrug DiscoverymedicineAnimalsHumansIC50Protein Kinase Inhibitors030304 developmental biologyPharmacology0303 health sciencesbiology010405 organic chemistryChemistryKinaseTriazinesOrganic ChemistryGeneral Medicinemedicine.diseaseCyclin-Dependent Kinases0104 chemical sciencesLeukemiaPyrimidinesbiology.proteinCancer researchMolecular mechanismCyclin-dependent kinase 7Cyclin-Dependent Kinase-Activating KinaseEuropean journal of medicinal chemistry
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Computational Evaluation and In Vitro Validation of New Epidermal Growth Factor Receptor Inhibitors

2020

Background:The Epidermal Growth Factor Receptor (EGFR) is a transmembrane protein that acts as a receptor of extracellular protein ligands of the epidermal growth factor (EGF/ErbB) family. It has been shown that EGFR is overexpressed by many tumours and correlates with poor prognosis. Therefore, EGFR can be considered as a very interesting therapeutic target for the treatment of a large variety of cancers such as lung, ovarian, endometrial, gastric, bladder and breast cancers, cervical adenocarcinoma, malignant melanoma and glioblastoma.Methods:We have followed a structure-based virtual screening (SBVS) procedure with a library composed of several commercial collections of chemicals (615,46…

Cell SurvivalDrug Evaluation PreclinicalAntineoplastic Agents01 natural sciencesReceptor tyrosine kinaseStructure-Activity Relationship03 medical and health scienceschemistry.chemical_compound0302 clinical medicineErbBEpidermal growth factorCell Line TumorDrug DiscoverymedicineHumansEpidermal growth factor receptorPropidium iodideProtein Kinase InhibitorsCell ProliferationEGFR inhibitorsDose-Response Relationship DrugMolecular StructurebiologyCell growthChemistryGeneral Medicine0104 chemical sciencesErbB ReceptorsMolecular Docking Simulation010404 medicinal & biomolecular chemistry030220 oncology & carcinogenesisbiology.proteinCancer researchErlotinibDrug Screening Assays Antitumormedicine.drugCurrent Topics in Medicinal Chemistry
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Synthesis and antiproliferative activity of substituted 3[2-(1H-indol-3-yl)-1,3-thiazol-4-yl]-1H-pyrrolo[3,2-b]pyridines, marine alkaloid nortopsenti…

2014

A large number of indolyl-4-azaindolyl thiazoles, nortopsentin analogues, were conveniently synthesized. The antiproliferative activity of the new derivatives was examined against four human tumor cell lines with different histologic origin. Seven derivatives consistently reduced the growth of the experimental models independently of TP53 gene status and exhibited the highest activity against the malignant peritoneal mesothelioma (STO) cell line. The most active compound of this series acts as a CDK1 inhibitor, and was found to cause cell cycle arrest at G 2 /M phase, to induce apoptosis by preventing the phosphorylation of survivin in Thr 34 and to increase the cytotoxic activity of paclit…

Cell cycle checkpointCDK1 InhibitorsAntiproliferative Activity CDK1 Inhibitors Diffuse Malignant Peritoneal Mesothelioma Nortopsentin Analogues SurvivinPyridinesStereochemistrySurvivinDiffuse Malignant Peritoneal MesotheliomaAntineoplastic AgentsApoptosisAntiproliferative Activity; CDK1 Inhibitors; Diffuse Malignant Peritoneal Mesothelioma; Nortopsentin Analogues; SurvivinBiochemistryCell LineAntiproliferative ActivityStructure-Activity Relationshipchemistry.chemical_compoundDrug DiscoverySurvivinHumansCytotoxic T cellProtein Kinase InhibitorsCell ProliferationPharmacologyCyclin-dependent kinase 1AlkaloidOrganic ChemistrySettore CHIM/08 - Chimica FarmaceuticaPaclitaxelchemistryCell cultureApoptosisNortopsentin AnaloguesMolecular Medicine
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Delayed ageing through damage protection by the Arf/p53 pathway.

2007

The tumour-suppressor pathway formed by the alternative reading frame protein of the Cdkn2a locus (Arf) and by p53 (also called Trp53) plays a central part in the detection and elimination of cellular damage, and this constitutes the basis of its potent cancer protection activity. Similar to cancer, ageing also results from the accumulation of damage and, therefore, we have reasoned that Arf/p53 could have anti-ageing activity by alleviating the load of age-associated damage. Here we show that genetically manipulated mice with increased, but otherwise normally regulated, levels of Arf and p53 present strong cancer resistance and have decreased levels of ageing-associated damage. These obser…

Cell signalingAgingTime FactorsTumor suppressor geneLongevityBiologymedicine.disease_causeAntioxidantsTranscriptomeMiceCDKN2ANeoplasmsmedicineAnimalsCells CulturedCyclin-Dependent Kinase Inhibitor p16MultidisciplinaryCell cycleFibroblastsCell biologyOxidative StressAgeingDisease SusceptibilitySignal transductionTumor Suppressor Protein p53Oxidative stressNature
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Comparative analysis of virtual screening approaches in the search for novel EphA2 receptor antagonists

2015

The EphA2 receptor and its ephrin-A1 ligand form a key cell communication system, which has been found overexpressed in many cancer types and involved in tumor growth. Recent medicinal chemistry efforts have identified bile acid derivatives as low micromolar binders of the EphA2 receptor. However, these compounds suffer from poor physicochemical properties, hampering their use in vivo. The identification of compounds able to disrupt the EphA2-ephrin-A1 complex lacking the bile acid scaffold may lead to new pharmacological tools suitable for in vivo studies. To identify the most promising virtual screening (VS) protocol aimed at finding novel EphA2 antagonists, we investigated the ability of…

Cell signalingDatabases Pharmaceuticaldrug designPharmaceutical ScienceComputational biologyBiologyCrystallography X-RayMolecular Docking SimulationArticleAnalytical Chemistrylcsh:QD241-441Structure-Activity RelationshipUser-Computer Interfacelcsh:Organic chemistryPPI inhibitorsDrug Discoveryshape screeningStructure–activity relationshipPhysical and Theoretical ChemistryReceptorProtein Kinase InhibitorsVirtual screeningMolecular StructureDrug discoveryReceptor EphA2EphA2 antagonistOrganic ChemistryEphrin-A1virtual screeningEPH receptor A2C700Combinatorial chemistryMolecular Docking SimulationUniPR129Chemistry (miscellaneous)Docking (molecular)dockingMolecular Medicinepharmacophore search
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Endothelial transcriptomic changes induced by oxidized low density lipoprotein disclose an up-regulation of Jak-Stat pathway.

2015

Oxidized low density lipoproteins (oxLDLs) act as an etiological factor in the development of atherosclerosis by modifying the biological properties of endothelial cells through mechanisms of vascular inflammation. To deepen the oxLDL changes at cellular level, a transcriptomic analysis of human umbilical artery endothelial cells (HUAECs) treated with oxLDL was performed to identify the modified signaling pathways. Total RNA was isolated from HUAECs treated with oxLDL (100 μg/ml). Gene expression analysis was carried out using Affymetrix oligonucleotide microarrays. Biological pathway analysis was performed using Ingenuity Pathway Analysis software. Microarray assay demonstrated that oxLDL …

Cell signalingTime FactorsPhysiologyBlotting WesternBiologyReal-Time Polymerase Chain ReactionTransfectionGene Expression Regulation EnzymologicBiological pathwayTranscriptomeRNA interferenceGene expressionHuman Umbilical Vein Endothelial CellsHumansGene Regulatory NetworksProtein Kinase InhibitorsCells CulturedOligonucleotide Array Sequence AnalysisPharmacologyGene Expression ProfilingJAK-STAT signaling pathwaySTAT2 Transcription FactorJanus Kinase 1Janus Kinase 2Cell biologyEndothelial stem cellLipoproteins LDLSTAT1 Transcription FactorMolecular Medicinelipids (amino acids peptides and proteins)RNA InterferenceSignal transductionTranscriptomeSignal TransductionVascular pharmacology
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Single-cell cloning of colon cancer stem cells reveals a multi-lineage differentiation capacity.

2008

Colon carcinoma is one of the leading causes of death from cancer and is characterized by a heterogenic pool of cells with distinct differentiation patterns. Recently, it was reported that a population of undifferentiated cells from a primary tumor, so-called cancer stem cells (CSC), can reconstitute the original tumor on xenotransplantation. Here, we show that spheroid cultures of these colon CSCs contain expression of CD133, CD166, CD44, CD29, CD24, Lgr5, and nuclear β-catenin, which have all been suggested to mark the (cancer) stem cell population. More importantly, by using these spheroid cultures or freshly isolated tumor cells from multiple colon carcinomas, we now provide compelling…

Cellular differentiationPopulationmultilineage differentationCell SeparationAdenocarcinomaTissue Culture TechniquesPhosphatidylinositol 3-KinasesCancer stem cellBiomarkers TumormedicineHumansCell LineageeducationProtein Kinase InhibitorsPhosphoinositide-3 Kinase Inhibitorseducation.field_of_studyMultidisciplinarybiologyCD44LGR5Cell DifferentiationBiological Sciencesmedicine.diseasePrimary tumorCell biologyIsolated Tumor CellsColonic NeoplasmsNeoplastic Stem Cellsbiology.proteinStem cell
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MAP kinase p38 and its relation to T cell anergy and suppressor function of regulatory T cells

2008

Diverse regulatory T cell populations (Treg) are important for the control of self tolerance and immune homeostasis. These include naturally occurring CD4+CD25+ Treg (nTreg) and induced Treg (iTreg). Tolerogenic dendritic cells, modulated by IL-10, are able to convert peripheral T cells into iTreg. These are anergic and characterized by a G(1) cell cycle arrest, dependent on elevated levels of the cdk inhibitor p27(Kip1). Novel data revealed a distinct pattern of MAP kinase activation in iTreg different from clonal T cell anergy, with enhanced activation of the p38-MAPKAP-K2/3 pathway. p38 is involved in cell cycle control and its activity is a prerequisite for the induction and maintenance…

Clonal AnergyCell cycle checkpointClonal anergyRegulatory T cellT cellCell CycleCell BiologyBiologyCell cycleT-Lymphocytes Regulatoryp38 Mitogen-Activated Protein KinasesCell biologymedicine.anatomical_structuremedicineAnimalsHumansCytotoxic T cellIL-2 receptorAntigen-presenting cellMolecular BiologyCyclin-Dependent Kinase Inhibitor p27Developmental BiologyCell Cycle
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Proliferation state and polo-like kinase1 dependence of tumorigenic colon cancer cells.

2012

Abstract Tumor-initiating cells are responsible for tumor maintenance and relapse in solid and hematologic cancers. Although tumor-initiating cells were initially believed to be mainly quiescent, rapidly proliferating tumorigenic cells were found in breast cancer. In colon cancer, the proliferative activity of the tumorigenic population has not been defined, although it represents an essential parameter for the development of more effective therapeutic strategies. Here, we show that tumorigenic colon cancer cells can be found in a rapidly proliferating state in vitro and in vivo, both in human tumors and mouse xenografts. Inhibitors of polo-like kinase1 (Plk1), a mitotic kinase essential fo…

Colorectal cancerCancer stem cellscolorectal cancercell proliferationcell cycle.Cell Cycle ProteinsMice0302 clinical medicineMice Inbred NODAC133 AntigenRNA Small Interfering0303 health scienceseducation.field_of_studyPteridinesCell CycleCell cycleImmunohistochemistry3. Good healthMitochondriaGene Expression Regulation Neoplastic030220 oncology & carcinogenesisColonic NeoplasmsMolecular MedicineFemaleStem cellPopulationTransplantation HeterologousCell Growth ProcessesBiologyProtein Serine-Threonine KinasesPLK103 medical and health sciencesCancer stem cellAntigens CDCell Line TumorProto-Oncogene ProteinsmedicineAnimalsHumanseducationProtein Kinase Inhibitors030304 developmental biologyGlycoproteinsSettore MED/04 - Patologia GeneraleCell growthCell Biologymedicine.diseaseTumor progressionImmunologyCancer researchPeptidesDevelopmental BiologyStem cells (Dayton, Ohio)
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