Search results for "mTOR pathway"

showing 10 items of 226 documents

A miRNA181a/NFAT5 axis links impaired T cell tolerance induction with autoimmune type 1 diabetes.

2018

Molecular checkpoints that trigger the onset of islet autoimmunity or progression to human type 1 diabetes (T1D) are incompletely understood. Using T cells from children at an early stage of islet autoimmunity without clinical T1D, we find that a microRNA181a (miRNA181a)-mediated increase in signal strength of stimulation and costimulation links nuclear factor of activated T cells 5 (NFAT5) with impaired tolerance induction and autoimmune activation. We show that enhancing miRNA181a activity increases NFAT5 expression while inhibiting FOXP3+ regulatory T cell (Treg) induction in vitro. Accordingly, Treg induction is improved using T cells from NFAT5 knockout (NFAT5ko) animals, whereas alter…

CD4-Positive T-Lymphocytes0301 basic medicineRegulatory T cellBiologymedicine.disease_causeAutoimmunityMice03 medical and health sciencesNFAT5microRNAImmunogeneticsmedicineAnimalsHumansPI3K/AKT/mTOR pathwaygeographygeography.geographical_feature_categoryNFATC Transcription FactorsAntagomirsFOXP3Forkhead Transcription FactorsGeneral MedicineIsletMice Mutant StrainsMicroRNAsTolerance inductionDiabetes Mellitus Type 1030104 developmental biologymedicine.anatomical_structureCancer researchFemale
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In the literature: June 2018

2018

Poly (ADP-ribose) polymerase (PARP) inhibitors (PARPi) are a highly active family of compounds that have changed the scenario in ovarian and human epidermal growth factor receptor 2 (HER2) non-amplified breast cancer management in the recent years. Despite impressive clinical activity, a prolonged treatment with PARPi is frequently associated with acquired resistance to this therapy. The identification of mechanisms and strategies to overcome resistance are crucial. Bromodomain containing 4 (BRD4) is a member of the bromodomain and extraterminal (BET) protein family that facilitates oncogenic transcription. BRD4 is frequently amplified in high-grade serous ovarian cancer (HGSOC) and can be …

Cancer ResearchBRD4ARID1AliteratureRAD51BiologyNewsBromodomainOncologyCancer cellCancer researchbiology.proteinPTENEctopic expression1506PI3K/AKT/mTOR pathwayESMO Open
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Novel pathway in Bcr-Abl signal transduction involves Akt-independent, PLC-γ1-driven activation of mTOR/p70S6-kinase pathway

2009

In chronic myeloid leukemia, activation of the phosphoinositide 3-kinase (PI3K)/Akt pathway is crucial for survival and proliferation of leukemic cells. Essential downstream molecules involve mammalian target of rapamycin (mTOR) and S6-kinase. Here, we present a comprehensive analysis of the molecular events involved in activation of these key signaling pathways. We provide evidence for a previously unrecognized phospholipase C-gamma1 (PLC-gamma1)-controlled mechanism of mTOR/p70S6-kinase activation, which operates in parallel to the classical Akt-dependent machinery. Short-term imatinib treatment of Bcr-Abl-positive cells caused dephosphorylation of p70S6-K and S6-protein without inactivat…

Cancer ResearchBlotting WesternMedizinFusion Proteins bcr-ablApoptosisProtein Serine-Threonine KinasesBiologyPiperazinesMiceLeukemia Myelogenous Chronic BCR-ABL Positivehemic and lymphatic diseasesGeneticsAnimalsHumansRNA Small InterferingProtein Kinase InhibitorsMolecular BiologyProtein kinase BCAMKPI3K/AKT/mTOR pathwayPhospholipase C gammaCell growthKinaseTOR Serine-Threonine KinasesRPTORIntracellular Signaling Peptides and ProteinsRibosomal Protein S6 Kinases 70-kDaCell biologyEnzyme ActivationPyrimidinesBenzamidesembryonic structuresImatinib MesylateCancer researchPhosphorylationSignal transductionProto-Oncogene Proteins c-aktSignal TransductionOncogene
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Holo-APP and G-protein-mediated signaling are required for sAPPa-induced activation of the Akt survival pathway

2014

International audience; Accumulating evidence indicates that loss of physiologic amyloid precursor protein (APP) function leads to reduced neuronal plasticity, diminished synaptic signaling and enhanced susceptibility of neurons to cellular stress during brain aging. Here we investigated the neuroprotective function of the soluble APP ectodomain sAPPa (soluble APPa), which is generated by cleavage of APP by a-secretase along the non-amyloidogenic pathway. Recombinant sAPPa protected primary hippocampal neurons and SH-SY5Y neuroblastoma cells from cell death induced by trophic factor deprivation. We show that this protective effect is abrogated in neurons from APP-knockout animals and APP-de…

Cancer ResearchCell SurvivalADAM10Amino Acid MotifsImmunology[SDV.BC]Life Sciences [q-bio]/Cellular BiologyIn Vitro TechniquesHydroxamic AcidsHippocampusNeuroprotectionCell LineADAM10 ProteinAmyloid beta-Protein PrecursorMicePhosphatidylinositol 3-Kinases03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicinemental disordersAmyloid precursor proteinAnimalsHumansProtein kinase BPI3K/AKT/mTOR pathwayPhosphoinositide-3 Kinase Inhibitors030304 developmental biologyMice Knockout0303 health sciencesbiologyBiochemistry and Molecular BiologyMembrane ProteinsDipeptidesCell BiologyMolecular biologyRecombinant ProteinsMice Inbred C57BLADAM ProteinsPertussis Toxinbiology.proteinOriginal ArticleSynaptic signalingAmyloid Precursor Protein SecretasesNeuron deathProto-Oncogene Proteins c-aktAmyloid precursor protein secretase030217 neurology & neurosurgeryBiokemi och molekylärbiologiSignal Transduction
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Abstract 1690: Differential autophagy activation in KRAS and EGFR mutant lung adenocarcinomas.

2013

Abstract Lung cancer is the leading cause of cancer deaths in western countries, and adenocarcinomas (LADs) are the most frequent histological subtype. The aberrant activation of the kinases promotes plethora of tumorigenic processes, mainly through PI3K and MAPK oncogenic pathways leading to oncogene addiction. The activation of PI3K pathway deregulates mTOR, a master kinase for cell growth and autophagy. Autophagy can be pro- or anti- tumorigenic, however its roles in protecting tumors exposed to metabolic stress under chemotherapy are considered as a survival mechanism for the tumors leading to acquired resistance. Consequently, the inhibition of autophagy is an attractive therapy to pre…

Cancer ResearchCell growthKinaseAutophagyBECN1BiologyProtein degradationmedicine.disease_causeOncogene AddictionOncologyImmunologyCancer researchmedicineKRASPI3K/AKT/mTOR pathwayCancer Research
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Moguntinones--new selective inhibitors for the treatment of human colorectal cancer.

2014

Abstract 3-Indolyl and 3-azaindolyl-4-aryl maleimide derivatives, called moguntinones (MOG), have been selected for their ability to inhibit protein kinases associated with angiogenesis and induce apoptosis. Here, we characterize their mode of action and their potential clinical value in human colorectal cancer in vitro and in vivo. MOG-19 and MOG-13 were characterized in vitro using kinase, viability, and apoptosis assays in different human colon cancer (HT-29, HCT-116, Caco-2, and SW480) and normal colon cell lines (CCD-18Co, FHC, and HCoEpiC) alone or in combination with topoisomerase I inhibitors. Intracellular signaling pathways were analyzed by Western blotting. To determine their pot…

Cancer ResearchIndolesColorectal cancerAngiogenesisApoptosisBiologyPharmacologyMetastasisMaleimidesMiceIn vivomedicineAnimalsHumansPI3K/AKT/mTOR pathwayKinaseTOR Serine-Threonine Kinasesmedicine.diseaseXenograft Model Antitumor AssaysOncologyApoptosisSignal transductionCaco-2 CellsTopoisomerase I InhibitorsColorectal NeoplasmsHT29 CellsProto-Oncogene Proteins c-aktSignal TransductionMolecular cancer therapeutics
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Liver Transplantation for Unresectable Intrahepatic Cholangiocarcinoma: The Role of Sequencing Genetic Profiling

2021

Simple Summary Intrahepatic cholangiocarcinoma is a rare disease with increasing incidence and mortality still characterized by an insufficient clinical outcome. Growing attention has recently surrounded this disease, and liver transplantation has emerged as a novel curative treatment for cholangiocarcinoma, along with a better understanding of genetic alterations potentially capable of driving tumorigenesis. The aim of this paper is to present a clinical description of our case series of patients affected by intrahepatic cholangiocarcinoma and by mixed forms of hepatocellular and cholangiocellular carcinoma, together with a genomic profiling of mutations occurring in a panel of genes relev…

Cancer ResearchLiver tumorliver transplantationbusiness.industrymedicine.medical_treatmentWnt signaling pathwayCancerNeoplasms. Tumors. Oncology. Including cancer and carcinogensLiver transplantationmedicine.diseasemedicine.disease_causeArticlenext-generation sequencing.Oncologyintrahepatic cholangiocarcinomamedicineCancer researchnext-generation sequencingKRASCarcinogenesisbusinessPI3K/AKT/mTOR pathwayIntrahepatic CholangiocarcinomaRC254-282intrahepatic cholangiocarcinoma; liver transplantation; next-generation sequencingCancers
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In the literature: February 2020.

2020

The phosphatidylinositol-3-kinase (PI3K)/Akt and the mammalian target of rapamycin (mTOR) signaling pathways is one of the most frequently deregulated pathways in human cancers. This pathway controls multiple cellular processes, including metabolism, motility, proliferation, growth and survival. It can be aberrantly activated through multiple mechanisms, including diverse genomic alterations involving oncogenes and tumour suppressor genes.1 These alterations offer opportunities for therapeutic targeting of the pathway. PI3Kα protein complex is composed of regulatory (p85α) and catalytic (p110α) subunits. Pik3ca codes for p110α, which is the most frequently mutated oncogene across different …

Cancer ResearchOncogeneFulvestrantKinaseBiologyP110αmedicine.diseaseBreast cancerEditorialOncologymedicineCancer research1506Signal transductionProtein kinase BPI3K/AKT/mTOR pathwaymedicine.drugESMO open
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The dual PI3K/mTOR inhibitor PKI-587 enhances sensitivity to cetuximab in EGFR-resistant human head and neck cancer models

2014

Background:Cetuximab is the only targeted agent approved for the treatment of head and neck squamous cell carcinomas (HNSCC), but low response rates and disease progression are frequently reported. As the phosphoinositide 3-kinase (PI3K) and the mammalian target of rapamycin (mTOR) pathways have an important role in the pathogenesis of HNSCC, we investigated their involvement in cetuximab resistance.Methods:Different human squamous cancer cell lines sensitive or resistant to cetuximab were tested for the dual PI3K/mTOR inhibitor PF-05212384 (PKI-587), alone and in combination, both in vitro and in vivo.Results:Treatment with PKI-587 enhances sensitivity to cetuximab in vitro, even in the co…

Cancer ResearchPathologyCetuximabApoptosisHNSCCHNSCCMiceAntineoplastic Combined Chemotherapy ProtocolsNeoplasmPhosphoinositide-3 Kinase InhibitorsMice Inbred BALB CCetuximabCaspase 3TriazinesTOR Serine-Threonine KinasesCetuximab resistanceErbB ReceptorsOncologyHead and Neck NeoplasmsMonoclonalCarcinoma Squamous Cellmedicine.drugmedicine.medical_specialtyMorpholinesPI3K-mTOR inhibitorsMice NudeAntineoplastic AgentsBiologyAntibodies Monoclonal HumanizedCell Line TumorAutophagymedicineCarcinomaAnimalsHumansneoplasmsPI3K/AKT/mTOR pathwayCell Proliferationcetuximab resistanceSquamous Cell Carcinoma of Head and Necktarget therapyCell growthAutophagyCancermedicine.diseaseXenograft Model Antitumor Assaysdigestive system diseasesDrug Resistance NeoplasmPI3K7mTOR inhibitorsCancer researchTranslational TherapeuticsBritish Journal of Cancer
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Mcl-1 is an anti-apoptotic factor for human hepatocellular carcinoma

2005

Defects in apoptosis signaling in hepatocytes contribute to tumorigenesis in hepatocellular carcinoma (HCC). In addition, treatment with chemotherapeutic drugs is often ineffective in HCC patients due to the apoptosis resistance of cancer cells. Anti-apoptotic members of the Bcl-2 family, including myeloid cell leukemia-1 (Mcl-1), which regulate intrinsic apoptosis induction at the mito-chondrial level, are often overexpressed in human cancer, and are implicated with disease grade and prognosis. Yet, little is known about the role of Mcl-1 in HCC. In this study, we analyzed the relevance of Mcl-1 expression for the apop-tosis resistance of human HCC. Mcl-1 protein expression was considerabl…

Cancer ResearchProgrammed cell deathCarcinoma HepatocellularApoptosisBiologyPhosphatidylinositol 3-KinasesEpidermal growth factorhemic and lymphatic diseasesTumor Cells CulturedmedicineHumansneoplasmsProtein kinase BPI3K/AKT/mTOR pathwayAkt/PKB signaling pathwayGene Expression ProfilingLiver NeoplasmsIntrinsic apoptosisPrognosisdigestive system diseasesNeoplasm ProteinsProto-Oncogene Proteins c-bcl-2OncologyImmunologyCancer cellCancer researchMyeloid Cell Leukemia Sequence 1 ProteinHepatocyte growth factorProto-Oncogene Proteins c-aktmedicine.drugInternational Journal of Oncology
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