Search results for "MTOR"

showing 10 items of 275 documents

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
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Gentamicin alters Akt-expression and its activation in the guinea pig cochlea

2015

Gentamicin treatment induces hair cell death or survival in the inner ear. Besides the well-known toxic effects, the phosphatidylinositol-3 kinase/Akt (PI3K/Akt) pathway was found to be involved in cell protection. After gentamicin application, the spatiotemporal expression patterns of Akt and its activated form (p-Akt) were determined in male guinea pigs. A single dose of 0.1 mL gentamicin (4 mg/ear/animal) was intratympanically injected. The auditory brainstem responses (ABRs) were recorded prior to application and 1, 2 and 7 days afterward. At these three time points the cochleae (n=10 in each case) were removed, transferred to fixative and embedded in paraffin. Seven ears were used as u…

MaleGuinea PigsBiologyAndrologyEvoked Potentials Auditory Brain Stemotorhinolaryngologic diseasesmedicineAnimalsInner earProtein kinase BCochleaPI3K/AKT/mTOR pathwaySpiral ganglionGeneral NeuroscienceAuditory ThresholdAnatomyImmunohistochemistryCochleamedicine.anatomical_structureOrgan of CortiSpiral ligamentsense organsHair cellGentamicinsProto-Oncogene Proteins c-aktCentral Nervous System AgentsNeuroscience
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PI3K/AKT pathway mutations cause a spectrum of brain malformations from megalencephaly to focal cortical dysplasia

2015

Malformations of cortical development containing dysplastic neuronal and glial elements, including hemimegalencephaly and focal cortical dysplasia, are common causes of intractable paediatric epilepsy. In this study we performed multiplex targeted sequencing of 10 genes in the PI3K/AKT pathway on brain tissue from 33 children who underwent surgical resection of dysplastic cortex for the treatment of intractable epilepsy. Sequencing results were correlated with clinical, imaging, pathological and immunohistological phenotypes. We identified mosaic activating mutations in PIK3CA and AKT3 in this cohort, including cancer-associated hotspot PIK3CA mutations in dysplastic megalencephaly, hemimeg…

MaleHemimegalencephalyPathologymedicine.medical_specialtyAKT3HemimegalencephalyPhosphatidylinositol 3-KinasesmedicinePTENHumansMegalencephalyPI3K/AKT/mTOR pathwaybiologyBrainOriginal ArticlesCortical dysplasiamedicine.diseaseDEPDC5MegalencephalyMalformations of Cortical DevelopmentDysplasiabiology.proteinFemaleNeurology (clinical)Proto-Oncogene Proteins c-aktSignal Transduction
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Molecular mechanisms of carfilzomib-induced cardiotoxicity in mice and the emerging cardioprotective role of metformin

2019

AbstractCarfilzomib (Cfz), an irreversible proteasome inhibitor licensed for relapsed/refractory myeloma, is associated with cardiotoxicity in humans. We sought to establish the optimal protocol of Cfz-induced cardiac dysfunction, to investigate the underlying molecular-signaling and, based on the findings, to evaluate the cardioprotective potency of metformin (Met). Mice were randomized into protocols 1 and 2 (control and Cfz for 1 and 2 consecutive days, respectively); protocols 3 and 4 (control and alternate doses of Cfz for 6 and 14 days, respectively); protocols 5A and 5B (control and Cfz, intermittent doses on days 0, 1 [5A] and 0, 1, 7, and 8 [5B] for 13 days); protocols 6A and 6B (p…

MaleImmunologymTORC1AMP-Activated Protein Kinases030204 cardiovascular system & hematologyPharmacologyBiochemistryMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicinemedicineAnimalsHypoglycemic AgentsProtein Phosphatase 2Protein kinase BCardiotoxicitybiologybusiness.industryBortezomibCell BiologyHematologyCarfilzomibCardiotoxicityMetforminMetforminMice Inbred C57BLNitric oxide synthasechemistry030220 oncology & carcinogenesisProteasome inhibitorbiology.proteinbusinessOligopeptidesSignal Transductionmedicine.drugBlood
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Posttranslational modifications by ADAM10 shape myeloid antigen-presenting cell homeostasis in the splenic marginal zone

2021

The spleen contains phenotypically and functionally distinct conventional dendritic cell (cDC) subpopulations, termed cDC1 and cDC2, which each can be divided into several smaller and less well-characterized subsets. Despite advances in understanding the complexity of cDC ontogeny by transcriptional programming, the significance of posttranslational modifications in controlling tissue-specific cDC subset immunobiology remains elusive. Here, we identified the cell-surface–expressed A-disintegrin-and-metalloproteinase 10 (ADAM10) as an essential regulator of cDC1 and cDC2 homeostasis in the splenic marginal zone (MZ). Mice with a CD11c-specific deletion of ADAM10 (ADAM10(ΔCD11c)) exhibited a …

MaleLangerinLymphoid TissueNotch signaling pathwayAntigen-Presenting CellsCD11cSpleenADAM10 ProteinMicePhosphatidylinositol 3-KinasesmedicineAnimalsHomeostasisMyeloid CellsProtein kinase BPI3K/AKT/mTOR pathwayCell ProliferationMultidisciplinarybiologyMacrophagesMembrane ProteinsCell DifferentiationDendritic CellsBiological SciencesCD11c AntigenCell biologyMice Inbred C57BLmedicine.anatomical_structurebiology.proteinFemaleAmyloid Precursor Protein SecretasesSignal transductionProtein Processing Post-TranslationalSpleenConventional Dendritic CellSignal TransductionProceedings of the National Academy of Sciences
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Roles of the Raf/MEK/ERK and PI3K/PTEN/Akt/mtor pathways in controlling growth and sensitivity to therapy-implications for cancer and aging

2011

Dysregulated signaling through the Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR pathways is often the result of genetic alterations in critical components in these pathways or upstream activators. Unrestricted cellular proliferation and decreased sensitivity to apoptotic-inducing agents are typically associated with activation of these pro-survival pathways. This review discusses the functions these pathways have in normal and neoplastic tissue growth and how they contribute to resistance to apoptotic stimuli. Crosstalk and commonly identified mutations that occur within these pathways that contribute to abnormal activation and cancer growth will also be addressed. Finally the recently described …

MaleMAPK/ERK pathwayAgingMAP Kinase Signaling SystemCancer aging RAF MEK mTORApoptosisReviewBiologyPI3KModels BiologicalApoptosis; Cancer; Kinases; MEK; MTOR; PI3K; Protein phosphorylation; RAF; Signal transductionMicePhosphatidylinositol 3-Kinases03 medical and health sciences0302 clinical medicineCancer stem cellNeoplasmscancerAnimalsHumansPTENProtein kinase BCellular SenescencePI3K/AKT/mTOR pathwayCell Proliferation030304 developmental biology0303 health sciencesKinaseTOR Serine-Threonine KinasesapoptosisPTEN PhosphohydrolaseRafCell BiologyMEKprotein phosphorylation3. Good healthCell biologyCrosstalk (biology)kinases030220 oncology & carcinogenesisMutationmTORCancer researchbiology.proteinFemaleraf KinasesProto-Oncogene Proteins c-aktCell agingsignal transduction
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Hormone replacement therapy enhances IGF-1 signaling in skeletal muscle by diminishing miR-182 and miR-223 expressions : a study on postmenopausal mo…

2014

MiRNAs are fine-tuning modifiers of skeletal muscle regulation, but knowledge of their hormonal control is lacking. We used a co-twin case-control study design, that is, monozygotic postmenopausal twin pairs discordant for estrogen-based hormone replacement therapy (HRT) to explore estrogen-dependent skeletal muscle regulation via miRNAs. MiRNA profiles were determined from vastus lateralis muscle of nine healthy 54-62-years-old monozygotic female twin pairs discordant for HRT (median 7 years). MCF-7 cells, human myoblast cultures and mouse muscle experiments were used to confirm estrogen's causal role on the expression of specific miRNAs, their target mRNAs and proteins and finally the act…

MaleMICRORNASMonozygotic twinmenopausePATHWAYMice0302 clinical medicineMyocyteInsulin-Like Growth Factor IIN-VIVO0303 health sciencesphosphorylationAge FactorsBREAST-CANCER CELLSWOMENMiddle Aged3142 Public health care science environmental and occupational healthPostmenopauseESTROGENmedicine.anatomical_structureMCF-7 CellsmTORGROWTHFemaleAUTOPHAGYMESSENGER-RNASignal TransductionIGF-1 receptormedicine.medical_specialtyHormone Replacement Therapymedicine.drug_classmiR-142-3pBiology03 medical and health sciencesInternal medicinemicroRNAmedicineAnimalsHumansMuscle SkeletalProtein kinase BPI3K/AKT/mTOR pathwayAged030304 developmental biologyAKTagingSkeletal muscleOriginal ArticlesTwins MonozygoticCell BiologyAKT; FOXO3A; IGF-1 signaling; IGF-1R; aging; mTOR; menopause; miR-142-3p; miR-182; miR-223; phosphorylationmiR-223EndocrinologyEstrogenCase-Control StudiesmiR-1823121 General medicine internal medicine and other clinical medicineFOXO3AIGF-1 signalingIGF-1R030217 neurology & neurosurgeryHUMAN LONGEVITYHormone
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Roles of signaling pathways in drug resistance, cancer initiating cells and cancer progression and metastasis

2014

The EGFR/PI3K/PTEN/Akt/mTORC pathway plays prominent roles in malignant transformation, prevention of apoptosis, drug resistance, cancer initiating cells (CICs) and metastasis. The expression of this pathway is frequently altered in breast and other cancers due to mutations at or aberrant expression of: HER2, EGFR1, PIK3CA, and PTEN as well as other oncogenes and tumor suppressor genes. miRs and epigenetic mechanisms of gene regulation are also important events which regulate this pathway. In some breast cancer cases, mutations at certain components of this pathway (e.g., PIK3CA) are associated with a better prognosis than breast cancers lacking these mutations. The expression of this pathw…

MaleOncologyCancer Researchmedicine.medical_treatmentTargeted therapyMetastasisTargeted therapyBreast cancerNeoplasmsNeoplasm MetastasisCancer stem cellsMedicine (all)Neoplasm ProteinsNeoplasm MetastasiGene Expression Regulation NeoplasticCell Transformation NeoplasticMolecular MedicineFemaleHormonal therapyHumanSignal Transductionmedicine.medical_specialtyEGFRBiologyNeoplasm ProteinBreast cancerGeneticCancer stem cellInternal medicineHER2GeneticsmedicineAnimalsHumansPTENMolecular BiologyProtein kinase BPI3K/AKT/mTOR pathwayCell ProliferationAnimalCancer stem cellTherapy resistanceCancermedicine.diseaseERDrug Resistance NeoplasmBreast cancer; Cancer stem cells; EGFR; ER; HER2; Hormonal therapy; Targeted therapy; Therapy resistancebiology.proteinCancer researchNeoplasm
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Bone morphogenetic protein 4 induces differentiation of colorectal cancer stem cells and increases their response to chemotherapy in mice.

2010

BACKGROUND & AIMS: The limited clinical response observed in many patients with colorectal cancer may be related to the presence of chemoresistant colorectal can- cer stem cells (CRC-SCs). Bone morphogenetic protein 4 (BMP4) promotes the differentiation of normal colonic stem cells. We investigated whether BMP4 might be used to induce differentiation of CRC-SCs and for therapeutic purposes. METHODS: CRC-SCs were isolated from 25 tumor samples based on expression of CD133 or using a selection culture medium. BMP4 expression and activity on CRC-SCs were evaluated in vitro; progeny of the stem cells were evaluated by immunofluorescence, immuno- blot, and flow cytometry analyses. The potential …

MaleOrganoplatinum CompoundsCellular differentiationDrug ResistanceApoptosisBone Morphogenetic Protein 4Colon Cancer; Drug Resistance; Neoplasia; Tumor Resistance to Chemotherapy; AC133 Antigen; Adenomatous Polyposis Coli; Aged; Aged 80 and over; Animals; Antigens CD; Antineoplastic Agents; Apoptosis; Bone Morphogenetic Protein 4; Cell Differentiation; Cells Cultured; Colorectal Neoplasms; Female; Fluorouracil; Glycoproteins; Humans; Male; Mice; Microsatellite Instability; Middle Aged; Mutation; Neoplastic Stem Cells; Organoplatinum Compounds; PTEN Phosphohydrolase; Peptides; Phosphatidylinositol 3-Kinase; Proto-Oncogene Proteins c-akt; Smad4 Protein; GastroenterologyMice80 and overBone morphogenetic protein receptorAC133 AntigenCells CulturedSmad4 ProteinAged 80 and overCulturedColon Cancerintegumentary systemGastroenterologyCell DifferentiationBMP4 colon stem cellsMiddle AgedCDOxaliplatinTumor Resistance to ChemotherapyBone morphogenetic protein 4Adenomatous Polyposis Coliembryonic structuresNeoplastic Stem CellsFemaleMicrosatellite InstabilityFluorouracilStem cellColorectal Neoplasmsanimal structuresCellsAntineoplastic AgentsBiologyBone morphogenetic proteinSettore MED/04 - PATOLOGIA GENERALECancer stem cellAntigens CDPTENAnimalsHumansAntigensneoplasmsPI3K/AKT/mTOR pathwayAgedGlycoproteinsNeoplasiaHepatologyPTEN Phosphohydrolasedigestive system diseasesMutationCancer researchbiology.proteinPhosphatidylinositol 3-KinasePeptidesProto-Oncogene Proteins c-aktGastroenterology
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Cytotoxic activity of the novel small molecule AKT inhibitor SC66 in hepatocellular carcinoma cells

2014

Hepatocellular carcinoma (HCC) is characterized by limited response to current drug therapies. Here, we report that SC66, a novel AKT inhibitor, reduced cell viability in a dose- and time-dependent manner, inhibited colony formation and induced apoptosis in HCC cells. SC66 treatment led to a reduction in total and phospho-AKT levels. This was associated with alterations in cytoskeleton organization, a reduction in expression levels of E-cadherin, β-catenin and phospho-FAK, together with up-regulation of Snail protein levels. All these alterations were coupled with anoikis cell death induction. In addition, SC66 induced the production of reactive oxygen species (ROS) and DNA damage. Pre-trea…

MaleProgrammed cell deathCarcinoma HepatocellularCytoskeleton organizationPyridinesMice NudeApoptosisBiologyMice03 medical and health sciences0302 clinical medicineanoikisCell Line TumorAnimalsHumansAnoikisViability assayHCCProtein Kinase InhibitorsProtein kinase BPI3K/AKT/mTOR pathwayCell Proliferation030304 developmental biologySC660303 health sciencesCyclohexanonesCell growthAKTLiver NeoplasmsXenograft Model Antitumor AssaysMolecular biology3. Good healthOncologyApoptosis030220 oncology & carcinogenesismTORCancer researchHCC AKT mTOR SC66 anoikisProto-Oncogene Proteins c-aktResearch Paper
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