Search results for "protein kinase inhibitor"

showing 10 items of 216 documents

Trimeric Hemibastadin Congener from the Marine Sponge Ianthella basta

2012

The first naturally occurring trimeric hemibastadin congener, sesquibastadin 1 (1), and the previously reported bastadins 3, 6, 7, 11, and 16 (2-6) were isolated from the marine sponge Ianthella basta, collected in Indonesia. The structure of 1 was elucidated on the basis of 1D and 2D NMR measurements and by HRMS. Among all the isolated compounds, the linear sesquibastadin 1 (1) and bastadin 3 (2) showed the strongest inhibition rates for at least 22 protein kinases (IC(50) = 0.1-6.5 μM), while the macrocyclic bastadins (3-6) demonstrated a strong cytotoxic potential against the murine lymphoma cell line L5178Y (IC(50) = 1.5-5.3 μM).

StereochemistryPharmaceutical ScienceMarine BiologySesquibastadinAnalytical ChemistryMiceIanthella bastaDrug DiscoveryHalogenated Diphenyl EthersAnimalsNuclear Magnetic Resonance BiomolecularProtein Kinase InhibitorsPharmacologyMolecular StructurebiologyMurine lymphomaOrganic Chemistrybiology.organism_classificationPoriferaSpongeCongenerComplementary and alternative medicineIndonesiaMolecular MedicineDrug Screening Assays AntitumorTwo-dimensional nuclear magnetic resonance spectroscopyJournal of Natural Products
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The high-performance technology CRISPR/Cas9 improves knowledge and management of acute myeloid leukemia

2021

Knowledge on acute myeloid leukemia pathogenesis and treatment has progressed recently, but not enough to provide ideal management. Improving the prognosis of acute myeloid leukemia patients depends on advances in molecular biology for the detection of new therapeutic targets and the production of effective drugs. The CRISPR/Cas9 technology allows gene insertions and deletions and it is the first step in investigating the function of their encoded proteins. Thus, new experimental models have been developed and progress has been made in understanding protein metabolism, antitumor activity, leukemic cell maintenance, differentiation, growth, apoptosis, and self-renewal, the combined pathogene…

TechnologyCD38acute myeloid leukemiamedicine.disease_causeGeneral Biochemistry Genetics and Molecular Biologycd38bcl2chemistry.chemical_compoundcrispr/cas9flt3 inhibitorshemic and lymphatic diseasesmedicineCRISPRHumansMidostaurinProtein Kinase InhibitorsCell ProliferationMutationCas9business.industryCell growthRMyeloid leukemiamedicine.diseaseidh2LeukemiaLeukemia Myeloid Acutechemistryfms-Like Tyrosine Kinase 3MutationCancer researchMedicineCRISPR-Cas SystemsbusinessBiomedical Papers
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Paclitaxel and beta-lapachone synergistically induce apoptosis in human retinoblastoma Y79 cells by downregulating the levels of phospho-Akt.

2009

Paclitaxel (PTX) and beta-lapachone (LPC) are naturally occurring compounds that have shown a large spectrum of anticancer activity. In this article we show for the first time that PTX/LPC combination induces potent synergistic apoptotic effects in human retinoblastoma Y79 cells. Combination of suboptimal doses of PTX (0.3 nM) and LPC (1.5 microM) caused biochemical and morphological signs of apoptosis at 48 h of treatment. These effects were accompanied by potent lowering in inhibitor of apoptosis proteins and by activation of Bid and caspases 3 and 6 with lamin B and PARP breakdown. PTX/LPC combination acted by favoring p53 stabilization through a lowering in p-Akt levels and in ps166-MDM…

Time FactorsPhysiologyClinical BiochemistryApoptosisInhibitor of Apoptosis ProteinsWortmanninchemistry.chemical_compoundSettore BIO/10 - BiochimicaAntineoplastic Combined Chemotherapy ProtocolsPhosphorylationCaspasebiologyCaspase 6Lamin Type BCaspase 3Protein StabilityRetinoblastomaDrug SynergismProto-Oncogene Proteins c-mdm2TransfectionBiochemistrylipids (amino acids peptides and proteins)Poly(ADP-ribose) PolymerasesWortmanninBH3 Interacting Domain Death Agonist Proteinretinoblastoma survival factors apoptosisPaclitaxelCell SurvivalPoly ADP ribose polymeraseActive Transport Cell NucleusDown-RegulationInhibitor of apoptosisTransfectionCell Line TumorHumansProtein kinase BProtein Kinase InhibitorsCell NucleusDose-Response Relationship DrugCell BiologyAntineoplastic Agents PhytogenicAndrostadieneschemistryCell cultureApoptosisbiology.proteinCancer researchTumor Suppressor Protein p53Proto-Oncogene Proteins c-aktNaphthoquinonesJournal of cellular physiology
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Enzymatically hydrolyzed low-density lipoprotein modulates inflammatory responses in endothelial cells

2009

SummaryThere is evidence that low-density lipoprotein (LDL) is modified by hydrolytic enzymes,and that the product (E-LDL) induces selective production of interleukin 8 (IL-8) in endothelial cells. Since nuclear factor-kappaB (NF-κB) is a major regulator of IL-8 transcription, we studied its activation in endothelial cells treated with E-LDL. Unexpectedly,the modified lipoprotein not only failed to activate NF-κB, but completely blocked its activation by tumour necrosis factor-alpha (TNF-α) in EA.hy926-cells, as assessed by electrophoretic mobility shift assays and immunofluorescence. Inhibition occurred upstream of NF-κB translocation, as inhibitor of NF-κB- (IκB)-phosphorylation was suppr…

Time FactorsProto-Oncogene Proteins c-junPyridinesmedicine.medical_treatmentFatty Acids NonesterifiedBiologyp38 Mitogen-Activated Protein KinasesCell Linechemistry.chemical_compoundNF-KappaB Inhibitor alphamedicineHumansTrypsinInterleukin 8PhosphorylationPromoter Regions GeneticProtein Kinase InhibitorsTranscription factorInflammationTumor Necrosis Factor-alphaActivator (genetics)HydrolysisInterleukin-8ImidazolesTranscription Factor RelAEndothelial CellsNF-κBHematologySterol EsteraseMolecular biologyLipoproteins LDLTranscription Factor AP-1Endothelial stem cellCytokineBiochemistrychemistryLow-density lipoproteinI-kappa B ProteinsLipoproteinThrombosis and Haemostasis
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Epigenetic activation of a cryptic TBC1D16 transcript enhances melanoma progression by targeting EGFR

2015

Metastasis is respoMetastasis is responsible for most cancer-related deaths, and, among common tumor types, melanoma is one with great potential to metastasize. Here we study the contribution of epigenetic changes to the dissemination process by analyzing the changes that occur at the DNA methylation level between primary cancer cells and metastases. We found a hypomethylation event that reactivates a cryptic transcript of the Rab GTPase activating protein TBC1D16 (TBC1D16-47 kDa; referred to hereafter as TBC1D16-47KD) to be a characteristic feature of the metastatic cascade. This short isoform of TBC1D16 exacerbates melanoma growth and metastasis both in vitro and in vivo. By combining imm…

Transcriptional ActivationGTPase-activating proteinImmunoprecipitationMice NudeEditorials: Cell Cycle FeaturesBiologyBioinformaticsMethylationGeneral Biochemistry Genetics and Molecular BiologyEpigenesis GeneticMetastasisMetastasisEpigènesiMetàstasiCell Line TumormedicineAnimalsImmunoprecipitationProtein IsoformsRNA MessengerEpigeneticsNeoplasm MetastasisRNA Small InterferingPromoter Regions GeneticProteïnes supressores de tumorsProtein Kinase InhibitorsMelanomaMelanomaGTPase-Activating ProteinsGeneral MedicineMethylationDNA MethylationPrognosismedicine.diseaseTumor suppressor proteinErbB ReceptorsMolecular WeightTreatment Outcomerab GTP-Binding ProteinsDNA methylationDisease ProgressionCancer researchRabMetilacióProtein BindingSignal TransductionEpigenesisNature Medicine
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Regulation of the tumor marker Fascin by the viral oncoprotein Tax of human T-cell leukemia virus type 1 (HTLV-1) depends on promoter activation and …

2015

AbstractAdult T-cell leukemia/lymphoma is a highly infiltrative neoplasia of CD4+ T-lymphocytes that occurs in about 5% of carriers infected with the deltaretrovirus human T-cell leukemia virus type 1 (HTLV-1). The viral oncoprotein Tax perturbs cellular signaling pathways leading to upregulation of host cell factors, amongst them the actin-bundling protein Fascin, an invasion marker of several types of cancer. However, transcriptional regulation of Fascin by Tax is poorly understood. In this study, we identified a triple mode of transcriptional induction of Fascin by Tax, which requires (1) NF-κB-dependent promoter activation, (2) a Tax-responsive region in the Fascin promoter, and (3) a p…

Transcriptional ActivationT-LymphocytesTaxmacromolecular substancesBiologyModels BiologicalFascinDownregulation and upregulationVirologyTranscriptional regulationmedicineHumansPromoter Regions GeneticProtein Kinase InhibitorsOncogeneFascinRegulation of gene expressionHuman T-lymphotropic virus 1NF‐kappa B (NF‐KB)Microfilament ProteinsNF-kappa BPromoterTumor virusTranscription regulationGene Products taxmedicine.diseasebiology.organism_classificationCell Transformation ViralPP2DeltaretrovirusLeukemiasrc-Family KinasesGene Expression RegulationHTLV-1ATLHuman T-lymphotropic virus 1Cancer researchbiology.proteinSignal transductionCarrier ProteinsSignal TransductionVirology
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Histamine Upregulates Gene Expression of Endothelial Nitric Oxide Synthase in Human Vascular Endothelial Cells

2003

Background— Histamine has a short-term, transient, stimulating effect on endothelial nitric oxide synthase (eNOS) activity; however, long-term effects on eNOS have not been described yet. In addition, the vascular effect of histamine seems to depend critically on eNOS functionality. Therefore, we studied the effects of histamine on eNOS gene expression and function. Methods and Results— In human umbilical vein endothelial cells (HUVECs) and HUVEC-derived EA.hy 926 cells, histamine upregulated eNOS mRNA (RNase protection assay) and protein (electron microscopic immunocytochemistry) expression. The upregulation of eNOS could be prevented by mepyramine, a selective antagonist at the H 1 recep…

Transcriptional Activationmedicine.medical_specialtyNitric Oxide Synthase Type IIIEndotheliumHistamine H1 receptorNitric OxideCell LineNitric oxidechemistry.chemical_compoundEnosPhysiology (medical)Internal medicinemedicineHumansRNA MessengerReceptors Histamine H1Enzyme InhibitorsPromoter Regions GeneticProtein Kinase InhibitorsCells CulturedDose-Response Relationship DrugbiologyNitric Oxide Synthase Type IIIbiology.organism_classificationMolecular biologyUp-RegulationNitric oxide synthaseKineticsOxidative StressEndocrinologymedicine.anatomical_structurechemistryEnzyme InductionCalcium-Calmodulin-Dependent Protein Kinasesbiology.proteinEndothelium VascularNitric Oxide SynthaseHistamine H3 receptorCalcium-Calmodulin-Dependent Protein Kinase Type 2Reactive Oxygen SpeciesCardiology and Cardiovascular MedicineHistamineHistamineCirculation
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MMP-10/stromelysin-2 promotes invasion of head and neck cancer.

2011

BackgroundPeriostin, IFN-induced transmembrane protein 1 (IFITM1) and Wingless-type MMTV integration site family, member 5B (Wnt-5b) were previously identified as the invasion promoted genes of head and neck squamous cell carcinoma (HNSCC) by comparing the gene expression profiles between parent and a highly invasive clone. We have previously reported that Periostin and IFITM1 promoted the invasion of HNSCC cells. Here we demonstrated that Wnt-5b overexpression promoted the invasion of HNSCC cells. Moreover, stromelysin-2 (matrix metalloproteinase-10; MMP-10) was identified as a common up-regulated gene among Periostin, IFITM1 and Wnt-5b overexpressing HNSCC cells by using microarray data s…

Tumor PhysiologyClone (cell biology)p38 Mitogen-Activated Protein KinasesMetastasisMetastasisMolecular Cell BiologyBasic Cancer ResearchNeoplasm MetastasisRegulation of gene expressionGene knockdownMultidisciplinaryHead and Neck cancerQRTransfectionHead and Neck TumorsExtracellular MatrixUp-RegulationGene Expression Regulation NeoplasticOncologyHead and Neck NeoplasmsGene Knockdown TechniquesCarcinoma Squamous CellMedicineResearch ArticleScience490Oral MedicineBiologyPeriostinHead and Neck Squamous Cell CarcinomaMatrix Metalloproteinase 10stomatognathic systemSettore MED/28 - Malattie OdontostomatologicheCell Line TumormedicineCancer Detection and Diagnosisotorhinolaryngologic diseasesHumansNeoplasm Invasiveness490BiologyExtracellular Matrix AdhesionsProtein Kinase InhibitorsneoplasmsMicroarray analysis techniquesCancers and Neoplasmsmedicine.diseaseMolecular biologyHead and neck squamous-cell carcinomaAntigens DifferentiationWnt Proteinsstomatognathic diseasesCancer researchCell Adhesion MoleculesPLoS ONE
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Acidic Environment Leads to ROS-Induced MAPK Signaling in Cancer Cells

2011

Tumor micromilieu often shows pronounced acidosis forcing cells to adapt their phenotype towards enhanced tumorigenesis induced by altered cellular signalling and transcriptional regulation. In the presents study mechanisms and potential consequences of the crosstalk between extra- and intracellular pH (pH(e), pH(i)) and mitogen-activated-protein-kinases (ERK1/2, p38) was analyzed. Data were obtained mainly in AT1 R-3327 prostate carcinoma cells, but the principle importance was confirmed in 5 other cell types. Extracellular acidosis leads to a rapid and sustained decrease of pH(i) in parallel to p38 phosphorylation in all cell types and to ERK1/2 phosphorylation in 3 of 6 cell types. Furth…

Tumor PhysiologyIntracellular Spacelcsh:MedicineSignal transductionERK signaling cascadeMolecular cell biologyNeoplasmsBasic Cancer ResearchTumor MicroenvironmentSignaling in Cellular ProcessesPhosphorylationCyclic AMP Response Element-Binding ProteinCreb Signalinglcsh:ScienceCellular Stress ResponsesMultidisciplinaryKinaseMechanisms of Signal TransductionSignaling cascadesHydrogen-Ion ConcentrationProtein-Tyrosine KinasesCell biologyOncologyMedicinePhosphorylationMitogen-Activated Protein KinasesSodium-Potassium-Exchanging ATPaseIntracellularResearch ArticleCell SurvivalMAP Kinase Signaling Systemp38 mitogen-activated protein kinasesIntracellular pHBiologyCREBModels BiologicalCell GrowthDogsCell Line TumorAnimalsHumansProtein Kinase InhibitorsBiologyPI3K/AKT/mTOR pathwaylcsh:RRatsEnzyme ActivationCancer cellbiology.proteinlcsh:QExtracellular SpaceReactive Oxygen SpeciesAcidsPLoS ONE
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Concomitant Use of Statins, Metformin, or Proton Pump Inhibitors in Patients with Advanced Renal Cell Carcinoma Treated with First-Line Combination T…

2022

Background Drug-drug interactions are a major concern in oncology and may potentially affect the outcome of patients with cancer. Objective In this study, we aimed to determine whether the concomitant use of statins, metformin, or proton pump inhibitors affects survival in patients with metastatic renal cell carcinoma treated with first-line combination therapies. Methods Medical records of patients with documented metastatic renal cell carcinoma between January 2016 and November 2021 were reviewed at 17 participating centers. This research was conducted in ten institutions, including both referral centers and local hospitals. Patients were assessed for overall survival, progression-free su…

Vascular Endothelial Growth Factor ACancer ResearchAngiogenesis InhibitorsProton Pump InhibitorsKidney NeoplasmsMetforminTreatment OutcomeOncologyHumansPharmacology (medical)Hydroxymethylglutaryl-CoA Reductase InhibitorsCarcinoma Renal CellProtein Kinase InhibitorsRetrospective StudiesTargeted oncology
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