Search results for "3-KINASE"

showing 10 items of 120 documents

Pharmacogenomic and molecular docking studies on the cytotoxicity of the natural steroid wortmannin against multidrug-resistant tumor cells

2014

Wortmannin is a cytotoxic compound derived from the endophytic fungi Fusarium oxysporum, Penicillium wortmannii and Penicillium funiculosum that occurs in many plants, including medicinal herbs. The rationale to develop novel anticancer drugs is the frequent development of tumor resistance to the existing antineoplasic agents. Therefore, it is mandatory to analyze resistance mechanisms of novel drug candidates such as wortmannin as well to bring effective drugs into the clinic that have the potential to bypass or overcome resistance to established drugs and to substantially increase life span of cancer patients. In the present project, we found that P-glycoprotein-overexpressing tumor cells…

DrugATP Binding Cassette Transporter Subfamily BClass I Phosphatidylinositol 3-Kinasesmedia_common.quotation_subjectPharmaceutical ScienceAntineoplastic AgentsATP-binding cassette transporterDrug resistancePharmacologyBiologyWortmanninPhosphatidylinositol 3-Kinaseschemistry.chemical_compoundCell Line TumorDrug DiscoveryCluster AnalysisHumansCytotoxicityProtein kinase BPI3K/AKT/mTOR pathwayOligonucleotide Array Sequence Analysismedia_commonPharmacologyDrug Resistance MultipleAndrostadienesMolecular Docking SimulationMultiple drug resistanceComplementary and alternative medicinechemistryDrug Resistance NeoplasmPharmacogeneticsMolecular MedicineWortmanninSignal TransductionPhytomedicine
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Extracellular Hsp70 Enhances Mesoangioblast Migration via an Autocrine Signaling Pathway

2016

Mouse mesoangioblasts are vessel-associated progenitor stem cells endowed with the ability of multipotent mesoderm differentiation. Therefore, they represent a promising tool in the regeneration of injured tissues. Several studies have demonstrated that homing of mesoangioblasts into blood and injured tissues are mainly controlled by cytokines/chemokines and other inflammatory factors. However, little is known about the molecular mechanisms regulating their ability to traverse the extracellular matrix (ECM). Here, we demonstrate that membrane vesicles released by mesoangioblasts contain Hsp70, and that the released Hsp70 is able to interact by an autocrine mechanism with Toll-like receptor …

Extracellular VesicleNF-kappa BEndothelial CellsModels BiologicalHsp70Toll-Like Receptor 4Autocrine CommunicationMicePhosphatidylinositol 3-KinasesMembrane MicrodomainsMatrix Metalloproteinase 9NF-KappaB Inhibitor alphaCell MovementMesoangioblast Stem CellAnimalsMatrix Metalloproteinase 2HSP70 Heat-Shock ProteinsExtracellular SpaceMatrix MetalloproteinaseProto-Oncogene Proteins c-aktLow Density Lipoprotein Receptor-Related Protein-1MigrationProtein BindingSignal Transduction
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MicroRNAs Associated With Biological Pathways of Left- and Right-sided Colorectal Cancer.

2020

BACKGROUND/AIM MicroRNAs (miRNAs) regulate the development of colorectal cancer (CRC). We aimed to investigate miRNAs and their relation to cancer-related signaling pathways in site-specific CRC. MATERIALS AND METHODS We used a total of 24 left- and right-sided Finnish CRC samples (discovery cohort) and The Cancer Genome Atlas public mature miRSeq dataset of 201 CRC samples (validation cohort). MiRNA differential expression and biological pathway analyses were performed using DESeq2 and the DIANA/mirPath tool, respectively. RESULTS We found 17 significantly differentially up-regulated [false discovery rate (FDR) <0.05] miRNAs in left-sided CRC ("left miRNAs"), and 15 in right-sided CRC ("ri…

False discovery rateOncologyMaleCancer Researchmedicine.medical_specialtyColorectal cancerDown-RegulationBiological pathwayCohort StudiesPhosphatidylinositol 3-KinasesTransforming Growth Factor betaInternal medicinemicroRNAMedicineHumansDifferential expressionPI3K/AKT/mTOR pathwayAgedbusiness.industryWnt signaling pathwayGeneral Medicinemedicine.diseasedigestive system diseasesUp-RegulationGene Expression Regulation NeoplasticOncologyCohortFemalebusinessColorectal NeoplasmsProto-Oncogene Proteins c-aktSignal TransductionAnticancer research
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Clinical and molecular data in cases of prenatal localized overgrowth disorder: major implication of genetic variants in PI3K‐AKT‐mTOR signaling path…

2021

To describe clinical and molecular findings in a French multicenter cohort of fetuses with prenatal diagnosis of congenital abnormality and suspicion of a localized overgrowth disorder (LOD) suggestive of genetic variants in the PI3K-AKT-mTOR signaling pathway.We analyzed retrospectively data obtained between 1 January 2013 and 1 May 2020 from fetuses with brain and/or limb overgrowth referred for molecular diagnosis of PI3K-AKT-mTOR pathway genes by next-generation sequencing (NGS) using pathological tissue obtained by fetal autopsy. We also assessed the diagnostic yield of amniotic fluid.During the study period, 21 subjects with LOD suspected of being secondary to a genetic variant of the…

HemimegalencephalyPathologymedicine.medical_specialtyGenetic counselingPrenatal diagnosisGermlineAKT3Phosphatidylinositol 3-KinasesHumansMedicineRadiology Nuclear Medicine and imagingMegalencephalyPI3K/AKT/mTOR pathwayRetrospective StudiesFetusRadiological and Ultrasound Technologybusiness.industryTOR Serine-Threonine KinasesObstetrics and GynecologyGeneral Medicinemedicine.diseaseReproductive MedicineMutationbusinessProto-Oncogene Proteins c-aktSignal TransductionUltrasound in Obstetrics &amp; Gynecology
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Endothelial Nitric Oxide Synthase Regulates T Cell Receptor Signaling at the Immunological Synapse

2006

The role of nitric oxide (NO) in T cells remains controversial, and the origin and localization of endogenous NO and whether it regulates lymphocyte activation are unclear. We show here that, within minutes of binding to antigen, T cells produce NO via endothelial nitric oxide synthase (eNOS). This process required increased intracellular Ca2+ and phosphoinositide3-kinase activity. By using an eNOS-green fluorescent fusion protein and fluorescent probes to detect NO, we show that eNOS translocates with the Golgi apparatus to the immune synapse of T helper cells engaged with antigen-presenting cells (APC), where it was fully activated. Overexpression of eNOS prevented the central coalescence…

Interleukin 2CD3 ComplexNitric Oxide Synthase Type IIIT-LymphocytesImmunologyReceptors Antigen T-CellAntigen-Presenting CellsGolgi ApparatusBiologyLymphocyte ActivationNitric OxideNitric oxideImmunological synapseInterferon-gammaMicePhosphatidylinositol 3-Kinaseschemistry.chemical_compoundAntigenmedicineAnimalsHumansImmunology and AllergyCytotoxic T cellAntigensMOLIMMUNOAntigen-presenting cellNitric Oxide Synthase Type IIIMice Mutant StrainsCell biologyInfectious DiseaseschemistryInterleukin-2CalciumSignal transductionSignal Transductionmedicine.drugImmunity
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Expression of angiogenic regulators, VEGF and leptin, is regulated by the EGF/PI3K/STAT3 pathway in colorectal cancer cells.

2009

Both leptin and vascular endothelial growth factor (VEGF) are growth and angiogenic cytokines that are upregulated in different types of cancer and have been implicated in neoplastic progression. Here we investigated the molecular mechanism by which leptin and VEGF expression are regulated in colon cancer by epidermal growth factor (EGF). In colon cancer cell line HT-29, EGF induced the binding of signal transducer and activator transcription 3 (STAT3) to STAT3 consensus motifs within the VEGF and leptin promoters and stimulated leptin and VEGF mRNA and protein synthesis. All these EGF effects were significantly blocked when HT-29 cells were treated with an inhibitor of the phosphoinositide…

LeptinSTAT3 Transcription FactorVascular Endothelial Growth Factor ASmall interfering RNAPhysiologyColorectal cancerClinical BiochemistryNeovascularization PhysiologicEGF/PI3K/STAT3colorectal cancerchemistry.chemical_compoundPhosphatidylinositol 3-KinasesEpidermal growth factormedicineHumansLY294002Gene SilencingRNA MessengerSTAT3Promoter Regions GeneticPI3K/AKT/mTOR pathwayCell NucleusbiologyEpidermal Growth FactorChemistryLeptinangiogenic regulators VEGF leptinCell Biologymedicine.diseaseUp-RegulationVascular endothelial growth factorGene Expression Regulation NeoplasticCancer researchbiology.proteinColorectal NeoplasmsHT29 Cellshormones hormone substitutes and hormone antagonistsProtein Binding
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Insulin-dependent leptin expression in breast cancer cells.

2008

Abstract Pathologic conditions associated with hyperinsulinemia, such as obesity, metabolic syndrome, and diabetes, seem to increase the risk of breast cancer. Here, we studied molecular mechanisms by which insulin activates the expression of leptin, an obesity hormone that has been shown to promote breast cancer progression in an autocrine or paracrine way. Using MDA-MB-231 breast cancer cells, we found that (a) insulin stimulated leptin mRNA and protein expression, which was associated with increased activation of the leptin gene promoter; (b) insulin increased nuclear accumulation of transcription factors hypoxia inducible factor (HIF)-1α and Sp1 and their loading on the leptin promoter;…

LeptinTranscriptional ActivationCancer Researchmedicine.medical_specialtySmall interfering RNAChromatin ImmunoprecipitationSp1 Transcription FactorBlotting WesternFluorescent Antibody TechniqueBreast NeoplasmsEnzyme-Linked Immunosorbent AssayBiologyParacrine signallingPhosphatidylinositol 3-Kinasesbreast cancerInternal medicinemedicineHyperinsulinemiaTumor Cells CulturedHumansHypoglycemic AgentsInsulinRNA MessengerRNA Small InterferingAutocrine signallingLuciferasesPromoter Regions GeneticTranscription factorCell NucleusMitogen-Activated Protein Kinase 1Gene knockdownLeptin receptorMitogen-Activated Protein Kinase 3Reverse Transcriptase Polymerase Chain ReactionLeptinmedicine.diseaseHypoxia-Inducible Factor 1 alpha SubunitCell HypoxiaEndocrinologyOncologyCancer researchFemalehormones hormone substitutes and hormone antagonistsCancer research
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Driver mutations and differential sensitivity to targeted therapies: a new approach to the treatment of lung adenocarcinoma

2010

The adenocarcinoma of the lung has recently shown peculiar molecular characteristics, which relate with both carcinogenesis and response to targeted drugs. Several molecular alterations have been defined as "driver mutations". These are responsible for both the initiation and maintenance of the malignancy. The epidermal growth factor receptor (EGFR) pathway is the main regulator of cell function and cancer development. It has a widely defined role in the occurrence of driver mutations. Up till now EGFR gene mutations, KRAS gene mutations and EML4-ALK fusion genes are the most widely recognized alterations involved in both the biology and the clinical management of lung adenocarcinoma. In th…

Lung NeoplasmsOncogene Proteins FusionSettore MED/06 - Oncologia MedicaEGFRGene ExpressionAdenocarcinomaGene mutationmedicine.disease_causeProto-Oncogene Proteins p21(ras)Phosphatidylinositol 3-KinasesPredictive Value of TestsProto-Oncogene ProteinsAntineoplastic Combined Chemotherapy ProtocolsmedicineAdenocarcinoma of the lungHumansRadiology Nuclear Medicine and imagingMolecular Targeted TherapyEpidermal growth factor receptorTyrosine kinase inhibitorsMutationbiologybusiness.industryDriver mutationGeneral MedicineProtein-Tyrosine KinasesPrognosismedicine.diseaseErbB ReceptorsTreatment OutcomeOncologyMutationImmunologyras ProteinsCancer researchbiology.proteinAdenocarcinomaKRASCarcinogenesisbusinessTyrosine kinaseAlgorithmsCancer Treatment Reviews
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Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR inhibitors: Rationale and importance to inhibiting these pathways in human health

2011

William H. Chappell 1 , Linda S. Steelman 1,2 , Jacquelyn M. Long 2 , Ruth C. Kempf 2 , Stephen L. Abrams 1 , Richard A. Franklin 1 , Jorg Basecke 3 , Franca Stivala 4 , Marco Donia 4 , Paolo Fagone 4 , Graziella Malaponte 4 , Maria C. Mazzarino 4 , Ferdinando Nicoletti 4 , Massimo Libra 4 , Danijela Maksimovic-Ivanic 5 , Sanja Mijatovic 5 , Giuseppe Montalto 6 , Melchiorre Cervello 7 , Piotr Laidler 8 , Michele Milella 9 , Agostino Tafuri 10 , Antonio Bonati 11 , Camilla Evangelisti 12 , Lucio Cocco 12 , Alberto M. Martelli 12,13 , and James A. McCubrey 1 1 Department of Microbiology and Immunology, Brody School of Medicine at East Carolina University 2 Department of Physics, Greenville, N…

MAPK/ERK pathwayAgingmedicine.medical_treatmentDrug ResistancerafPI3KTargeted therapycombination therapyPhosphatidylinositol 3-Kinases0302 clinical medicineTARGETED THERAPYCANCER STEM CELLSNeoplasmsCancer Stem CellsMedicineExtracellular Signal-Regulated MAP Kinases0303 health sciencesCombination TherapybiologyTOR Serine-Threonine KinasesMTORHuman health Ras inhibitors MEK ERKTargeted TherapyDiscovery and development of mTOR inhibitors3. Good healthDRUG RESISTANCECell Transformation NeoplasticOncology030220 oncology & carcinogenesismTORraf KinasesPremature agingMAP Kinase Signaling SystemReviewsSenescence03 medical and health sciencesCell Line TumorHumansPTENProtein kinase BPI3K/AKT/mTOR pathway030304 developmental biologyMitogen-Activated Protein Kinase Kinasesbusiness.industryAKTAktagingPTEN PhosphohydrolaseRafTransplantationSENESCENCEImmunologyras Proteinsbiology.proteinCancer researchaging; akt; cancer stem cells; combination therapy; drug resistance; mtor; pi3k; raf; senescence; targeted therapybusinessProto-Oncogene Proteins c-akt
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Evaluation and clinical analyses of downstream targets of the Akt inhibitor GDC-0068.

2013

Abstract Purpose: The oncogenic PI3K/Akt/mTOR pathway is an attractive therapeutic target in cancer. However, it is unknown whether the pathway blockade required for tumor growth inhibition is clinically achievable. Therefore, we conducted pharmacodynamic studies with GDC-0068, an ATP competitive, selective Akt1/2/3 inhibitor, in preclinical models and in patients treated with this compound. Experimental Design: We used a reverse phase protein array (RPPA) platform to identify a biomarker set indicative of Akt inhibition in cell lines and human-tumor xenografts, and correlated the degree of pathway inhibition with antitumor activity. Akt pathway activity was measured using this biomarker se…

MAPK/ERK pathwayCancer ResearchAKT1PharmacologyPiperazines03 medical and health sciencesMicePhosphatidylinositol 3-Kinases0302 clinical medicineIn vivoMedicineAnimalsHumansProtein kinase BProtein Kinase InhibitorsPI3K/AKT/mTOR pathway030304 developmental biology0303 health sciencesbusiness.industryTOR Serine-Threonine KinasesCancerReverse phase protein lysate microarraymedicine.diseaseXenograft Model Antitumor Assays3. Good healthOncogene Protein v-aktPyrimidinesOncology030220 oncology & carcinogenesisBiomarker (medicine)businessSignal TransductionClinical cancer research : an official journal of the American Association for Cancer Research
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