Search results for "Phosphoinositide"

showing 10 items of 40 documents

Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR cascade inhibitors: How mutations can result in therapy resistance and how to overcome resistance

2012

// James A. McCubrey 1 , Linda S. Steelman 1 , William H. Chappell 1 , Stephen L. Abrams 1 , Richard A. Franklin 1 , Giuseppe Montalto 2 , Melchiorre Cervello 3 , Massimo Libra 4 , Saverio Candido 4 , Grazia Malaponte 4 , Maria C. Mazzarino 4 , Paolo Fagone 4 , Ferdinando Nicoletti 4 , Jorg Basecke 5 , Sanja Mijatovic 6 , Danijela Maksimovic-Ivanic 6 , Michele Milella 7 , Agostino Tafuri 8 , Francesca Chiarini 9 , Camilla Evangelisti 9 , Lucio Cocco 10 , Alberto M. Martelli 9,10 1 Department of Microbiology and Immunology, Brody School of Medicine at East Carolina University, Greenville, NC, USA 2 Department of Internal Medicine and Specialties, University of Palermo, Palermo, Italy 3 Consi…

MAPK/ERK pathwaymedicine.medical_treatmentPI3KTargeted therapyTargeted therapyPhosphatidylinositol 3-Kinases0302 clinical medicineNeoplasmsTreatment resistanceExtracellular Signal-Regulated MAP KinasesPhosphoinositide-3 Kinase InhibitorsGenetics0303 health sciencesbiologyCancer stem cellsTOR Serine-Threonine KinasesMAP Kinase Kinase KinasesDiscovery and development of mTOR inhibitorshumanities3. Good healthOncology030220 oncology & carcinogenesismTORSignal TransductionProto-Oncogene Proteins B-rafReviewsAntineoplastic Agents03 medical and health sciencesCell Line TumormedicineHumansPTENProtein kinase BPI3K/AKT/mTOR pathway030304 developmental biologybusiness.industryAkt; Cancer stem cells; mTOR; PI3K; Raf; Targeted therapy; Therapy resistanceAktPTEN PhosphohydrolaseTherapy resistanceRafProtein phosphatase 2Targeted Therapy Therapy Resistance Cancer Stem Cells Raf Akt PI3K mTORDrug Resistance NeoplasmMutationras ProteinsCancer researchbiology.proteinbusinessProto-Oncogene Proteins c-akt
researchProduct

Synergistic Growth Inhibitory Activity of Combined Mek/Mtor Pathway Blockade in Pten-Null Cancers

2014

ABSTRACT Aim: We have recently shown that induction of PTEN expression plays an integral role in MEK inhibitors' antitumor activity. Here we hypothesize that PTEN status critically influences the functional outcome of combined MEK and PI3K/mTOR inhibition. Methods: Single and combined MEK (trametinib, T) and mTOR (everolimus, E) blockade were assessed in a panel of cancer cell lines and in patient-derived lung and colon cancer stem cells (L- or C-CSC). Pharmacologic interactions were analyzed by conservative isobologram analysis. PTEN role was assessed by shRNA-mediated silencing or overexpression by stable transfection. Treatment-induced changes in the phosphoproteome were analyzed by anti…

MEK/MTORMAPK/ERK pathwayTrametinibPhosphoinositide 3-kinasebiologyKinaseRPTORHematologyOncologySettore MED/04 - PATOLOGIA GENERALEbiology.proteinCancer researchPTENProtein kinase BPI3K/AKT/mTOR pathwayAnnals of Oncology
researchProduct

Colony-stimulating factor-1-induced oscillations in phosphatidylinositol-3 kinase/AKT are required for caspase activation in monocytes undergoing dif…

2009

Abstract The differentiation of human peripheral blood monocytes into resident macrophages is driven by colony-stimulating factor-1 (CSF-1), which upon interaction with CSF-1 receptor (CSF-1R) induces within minutes the phosphorylation of its cytoplasmic tyrosine residues and the activation of multiple signaling complexes. Caspase-8 and -3 are activated at day 2 to 3 and contribute to macrophage differentiation, for example, through cleavage of nucleophosmin. Here, we show that the phosphatidylinositol-3 kinase and the downstream serine/threonine kinase AKT connect CSF-1R activation to caspase-8 cleavage. Most importantly, we demonstrate that successive waves of AKT activation with increasi…

Macrophage colony-stimulating factorCellular differentiationImmunologyImmunoblottingApoptosisBiologyBiochemistryMonocytesImmunoenzyme TechniquesPhosphatidylinositol 3-KinasesHumansImmunoprecipitationRNA MessengerPhosphorylationProtein kinase BCells CulturedPhosphoinositide-3 Kinase InhibitorsMitogen-Activated Protein Kinase 1Caspase 8Mitogen-Activated Protein Kinase 3MAP kinase kinase kinaseKinaseAkt/PKB signaling pathwayReverse Transcriptase Polymerase Chain ReactionMacrophage Colony-Stimulating FactorMacrophagesCell DifferentiationCell BiologyHematologyFlow CytometryCell biologyEnzyme ActivationPhosphorylationSignal transductionProto-Oncogene Proteins c-aktSignal TransductionBlood
researchProduct

TGF-β Signaling Pathways in Different Compartments of the Lower Airways of Patients With Stable COPD

2017

Background: The expression and localization of transforming growth factor-β (TGF-β) pathway proteins in different compartments of the lower airways of patients with stable COPD is unclear. We aimed to determine TGF-β pathway protein expression in patients with stable COPD. Methods: The expression and localization of TGF-β pathway components was measured in the bronchial mucosa and peripheral lungs of patients with stable COPD (n = 44), control smokers with normal lung function (n = 24), and control nonsmoking subjects (n = 11) using immunohistochemical analysis. Results: TGF-β1, TGF-β3, and connective tissue growth factor expression were significantly decreased in the bronchiolar epithelium…

MaleCCN2 connective tissue growth factorSmad Proteinsairway inflammationCritical Care and Intensive Care MedicineTRAP-1 transforming growth factor-β receptor-associated binding proteinPulmonary Disease Chronic ObstructiveLAP latency-associated peptideSMAD small mother against decapentaplegicBAMBI CTGF SMAD TGF-B airway inflammation autoimmunityLungTGF transforming growth factorLLC large latent complexBAMBI CTGF SMAD TGF-β Airway Inflammation AutoimmunityautoimmunityMiddle Agedrespiratory systemLTBP latent transforming growth factor-β binding proteinImmunohistochemistryTGIF 5′-TG-3′-interacting factorECM extracellular matrixTGFBI transforming growth factor-β-induced proteinFemaleCardiology and Cardiovascular MedicinePI3K phosphoinositide 3-kinaseSignal TransductionTGF-βPulmonary and Respiratory MedicineTGF-βR TGF-β receptorSocio-culturaleBronchiRespiratory MucosaArticleTGF-BTransforming Growth Factor beta1Transforming Growth Factor beta3Macrophages AlveolarHumansAgedBAMBI; CTGF; SMAD; TGF-β; airway inflammation; autoimmunityBAMBIMembrane ProteinsCTGFBMP bone morphogenetic proteinBAMBI; CTG; SMAD; TGF-β; airway inflammation; autoimmunityCTGBAMBI bone morphogenetic proteins and activin membrane-bound inhibitorrespiratory tract diseasesairway inflammation; autoimmunity; BAMBI; CTGF; SMAD; TGF-β; Pulmonary and Respiratory Medicine; Critical Care and Intensive Care Medicine; Cardiology and Cardiovascular MedicineCase-Control StudiesBiomarkersMAPK mitogen-activated protein kinaseSMAD
researchProduct

Trastuzumab therapy vs tetracycline controlled ERBB2 downregulation: influence on tumour development in an ERBB2-dependent mouse tumour model

2008

Trastuzumab (Herceptin) has improved therapy of breast cancer. Only patients overexpressing ERBB2 are treated with trastuzumab, whereas its use in tumours without ERBB2 expression is useless. This led to the concept that the subgroup of trastuzumab-sensitive tumours is ‘ERBB2-dependent', meaning that ERBB2 signalling is indispensable for growth of these tumours. We used a mouse model that allows anhydrotetracycline (ATc)-controlled downregulation of ERBB2 in tumour tissue. ERBB2 mRNA and protein expression were downregulated below detection limit leading to a macroscopically complete tumour remission within 14 days. Tumour remission was accompanied by a strong decrease in proliferation, a m…

MaleCancer ResearchReceptor ErbB-2AKT1AKT2ApoptosisMiceTrastuzumabPKBskin and connective tissue diseasesERBB2Mitogen-Activated Protein Kinase 3biologyERK1/2herceptinAntibodies MonoclonalCytochromes cImmunohistochemistrynude miceGene Expression Regulation NeoplasticOncologyTetracyclinesKi-67Ki-67Femalemedicine.drugmedicine.medical_specialtyBlotting WesternDown-RegulationMice NudeAntineoplastic AgentsProtein Serine-Threonine KinasesAntibodies Monoclonal Humanizedresistance3-Phosphoinositide-Dependent Protein Kinasesbreast cancerDownregulation and upregulationresponse to therapyInternal medicineHER2medicineAnimalsRNA Messengercytochrome c releaseProtein kinase Bneoplasmstumour developmentCell Proliferationhumanised monoclonal antibodyAktCancerMammary Neoplasms ExperimentalTrastuzumabmedicine.diseaseEndocrinologyKi-67 AntigenApoptosisDrug Resistance Neoplasmbiology.proteinCancer researchreceptor tyrosine kinaseTranslational TherapeuticsProto-Oncogene Proteins c-aktBritish Journal of Cancer
researchProduct

miR-20b and miR-451a Are Involved in Gastric Carcinogenesis through the PI3K/AKT/mTOR Signaling Pathway: Data from Gastric Cancer Patients, Cell Line…

2020

Gastric cancer (GC) is one of the most common and lethal gastrointestinal malignancies worldwide. Many studies have shown that development of GC and other malignancies is mainly driven by alterations of cellular signaling pathways. MicroRNAs (miRNAs) are small noncoding molecules that function as tumor-suppressors or oncogenes, playing an essential role in a variety of fundamental biological processes. In order to understand the functional relevance of miRNA dysregulation, studies analyzing their target genes are of major importance. Here, we chose to analyze two miRNAs, miR-20b and miR-451a, shown to be deregulated in many different malignancies, including GC. Deregulated expression of miR…

MaleCell signalingAntagonists & inhibitorsCaveolin 1ApoptosisCatalysisTuberous Sclerosis Complex 1 ProteinArticleInorganic Chemistrylcsh:ChemistryMicePhosphatidylinositol 3-KinasesStomach NeoplasmsCell Line TumormicroRNAPTENAnimalsHumans616.33-006.6 [udc]Physical and Theoretical ChemistryMolecular BiologyProtein kinase Blcsh:QH301-705.5SpectroscopyPI3K/AKT/mTOR pathwaybiologyTOR Serine-Threonine Kinasesgastric cancerOrganic ChemistryPTEN PhosphohydrolaseAntagomirsGeneral MedicineStomach neoplasms ; genetics ; MicroRNAs ; genetics ; Phosphoinositide-3 Kinase Inhibitors ; Phosphatidylinositol 3-Kinase ; metabolism ; Proto-Oncogene Proteins c-akt ; antagonists&inhibitors ; Proto-Oncogene Proteins c-akt ; metabolism ; TOR Serine-Threonine Kinases ; antagonists&inhibitors ; TOR Serine-Threonine Kinases ; metabolism ; Signal transduction ; drug effects ; Disease models animal ; MicemiR-451aComputer Science ApplicationsmicroRNAsDisease Models Animallcsh:Biology (General)lcsh:QD1-999biology.proteinCancer researchFemalemiR-20bSignal transductionCarrier ProteinsProto-Oncogene Proteins c-aktTXNIPSignal TransductionPI3K/AKT/mTOR signaling pathwayInternational Journal of Molecular Sciences
researchProduct

Phospholipase D in rat myocardium: formation of lipid messengers and synergistic activation by G-protein and protein kinase C.

1998

Activation of phospholipase D (PLD) and phosphoinositide-specific phospholipase C (PI-PLC) by fluoride, to stimulate heterotrimeric G-proteins, and by phorbol esters, to stimulate protein kinase C (PKC), was studied in rat atria. Fluoride and 4beta-phorbol-12beta,13alpha-dibutyrate (PDB), in contrast to 4beta-phorbol-13alpha-acetate (PAc), activated PLD, catalyzing the formation of [3H]-phosphatidylethanol ([3H]-PETH), [3H]-phosphatidic acid ([3H]-PA), choline and sn-1,2-diacylglycerol (DAG). Basal PLD activity was resistant to drastic changes in Ca2+ and to Ro 31-8220, a PKC inhibitor, but was decreased by genistein, an inhibitor of tyrosine kinase, and increased by vanadate, a tyrosine ph…

MaleG proteinProtein tyrosine phosphataseBiologyBiochemistrySecond Messenger Systemschemistry.chemical_compoundPhosphoinositide Phospholipase CGTP-Binding ProteinsPhorbol EstersPhospholipase DAnimalsRats WistarProtein kinase CPhorbol 1213-DibutyrateProtein Kinase CDiacylglycerol kinasePharmacologyPhospholipase CPhospholipase DMyocardiumPhosphatidylinositol Diacylglycerol-LyaseTyrosine phosphorylationDrug SynergismLipid MetabolismLipidsRatsEnzyme ActivationBiochemistrychemistryType C PhospholipasesSecond messenger systemlipids (amino acids peptides and proteins)Biochemical pharmacology
researchProduct

The dark side of the moon: The PI3K/PTEN/AKT pathway in colorectal carcinoma

2009

Wild-type KRAS status is required but not sufficient to confer sensitivity to anti-epidermal growth factor receptor (EGFR) monoclonal antibodies (mAbs) in colorectal cancer patients. As a consequence, one of the major challenges is to identify, in non-mutant KRAS patients, other markers that can predict lack of response to this therapy. Small series have investigated the clinical effect of PIK3CA mutations on resistance to anti-EGFR mAbs and discrepant results have been observed. Furthermore, PTEN loss in metastases may be predictive of resistance to anti-EGFR mAbs, even if PTEN determination is far from an immediate clinical application. The introduction of modulators of the PI3K/AKT/mTOR …

PTENCancer ResearchClass I Phosphatidylinositol 3-KinasesPrognosiSettore MED/06 - Oncologia MedicaColorectal cancerCetuximabColorectal NeoplasmPhosphoinositide 3-kinasemedicine.disease_causePhosphatidylinositol 3-KinasesAntineoplastic Combined Chemotherapy ProtocolsBiomarkers TumormedicineHumansPTENPanitumumabEpidermal growth factor receptorProtein kinase BPI3K/AKT/mTOR pathwayClass I Phosphatidylinositol 3-KinaseAntineoplastic Combined Chemotherapy ProtocolbiologyCetuximabAKTMTORPanitumumabPTEN PhosphohydrolaseAntibodies MonoclonalGeneral MedicinePrognosismedicine.diseaseErbB ReceptorsOncologyMutationbiology.proteinCancer researchReceptor Epidermal Growth FactorKRASPhosphatidylinositol 3-KinaseColorectal NeoplasmsProto-Oncogene Proteins c-aktHumanSignal Transductionmedicine.drug
researchProduct

Pho85 and PI(4,5)P(2) regulate different lipid metabolic pathways in response to cold

2019

Lipid homeostasis allows cells to adjust membrane biophysical properties in response to changes in environmental conditions. In the yeast Saccharomyces cerevisiae, a downward shift in temperature from an optimal reduces membrane fluidity, which triggers a lipid remodeling of the plasma membrane. How changes in membrane fluidity are perceived, and how the abundance and composition of different lipid classes is properly balanced, remain largely unknown. Here, we show that the levels of phosphatidylinositol 4,5-bisphosphate [PI(4,5)P2], the most abundant plasma membrane phosphoinositide, drop rapidly in response to a downward shift in temperature. This change triggers a signaling cascade trans…

Phosphatidylinositol 45-DiphosphateSaccharomyces cerevisiae ProteinsMembrane FluiditySphingoid basesAcclimatizationOrm2PhospholipidSaccharomyces cerevisiaePhosphoinositideTriacylglycerideSphingolipidArticle03 medical and health scienceschemistry.chemical_compoundGlycogen Synthase Kinase 3Gene Expression Regulation FungalMembrane fluidityLow temperatureInositolPhosphatidylinositolProtein kinase AMolecular Biology1-IP7030304 developmental biology0303 health sciencesChemistry030302 biochemistry & molecular biologyCell MembraneCell BiologyLipid MetabolismSphingolipidCyclin-Dependent KinasesCell biologyTORC2-Pkh1-Ypk1 signaling moduleCold TemperatureCytosolMetabolic pathwayPhospholipidMetabolic Networks and PathwaysSignal Transduction
researchProduct

Control of cellular phosphatidylinositol 4,5-bisphosphate levels by adhesion signals and Rho GTPases in NIH 3T3 fibroblasts

2000

The involvement of small GTPases of the Rho family in the control of phosphoinositide metabolism by adhesion signals was examined in NIH 3T3 fibroblasts. Abrogation of adhesion signals by detachment of cells from their substratum resulted in a time-dependent decrease in the cellular level of PtdIns(4,5)P2 by approximately 50%. This effect could be mimicked by treatment of adherent cells with Clostridium difficile toxin B and toxin B-1470, which inhibit specific subsets of Rho and Ras GTPases. Detachment of cells that had been pretreated with the clostridial toxins did not cause a further reduction in PtdIns(4,5)P2 levels, suggesting that the target GTPases are integrated into the control of…

Phosphatidylinositol 45-Diphosphaterac1 GTP-Binding Proteinrho GTP-Binding ProteinsBacterial ToxinsCellClostridium difficile toxin BRAC1GTPasePhospholipaseBiologyTransfectionBiochemistryMicechemistry.chemical_compoundPhosphoinositide Phospholipase CBacterial ProteinsCell AdhesionmedicineAnimalsPhosphorylationInositol phosphatechemistry.chemical_classificationPhospholipase CCytotoxinsPhosphoric Diester Hydrolases3T3 CellsMolecular biologyRecombinant ProteinsCell biologyKineticsPhosphotransferases (Alcohol Group Acceptor)medicine.anatomical_structurechemistryPhosphatidylinositol 45-bisphosphateType C PhospholipasesCalciumSignal TransductionEuropean Journal of Biochemistry
researchProduct