Search results for "phosphatidylinositol 3-Kinases"

showing 10 items of 107 documents

A PTEN inhibitor displays preclinical activity against hepatocarcinoma cells

2016

Phosphatase and tensin homolog (PTEN) gene is considered a tumor suppressor gene. However, PTEN mutations rarely occur in hepatocellular carcinoma (HCC), whereas heterozygosity of PTEN, resulting in reduced PTEN expression, has been observed in 32–44% of HCC patients. In the present study, we investigated the effects of the small molecule PTEN inhibitor VO-OHpic in HCC cells. VO-OHpic inhibited cell viability, cell proliferation and colony formation, and induced senescence-associated β-galactosidase activity in Hep3B (low PTEN expression) and to a lesser extent in PLC/PRF/5 (high PTEN expression) cells, but not in PTEN-negative SNU475 cells. VO-OHpic synergistically inhibited cell viability…

0301 basic medicineMAPK/ERK pathwayPTENCarcinoma HepatocellularsenescenceTumor suppressor geneCell SurvivalMicePhosphatidylinositol 3-Kinases03 medical and health sciences0302 clinical medicineReportOrganometallic CompoundsAnimalsHumansPTENTensinViability assayHCCProtein kinase BMolecular BiologyPI3K/AKT/mTOR pathwayCell ProliferationbiologyCell growthTOR Serine-Threonine KinasesAKTLiver NeoplasmsPTEN PhosphohydrolaseCell BiologySorafenibXenograft Model Antitumor Assaysdigestive system diseasesVO-OHpicGene Expression Regulation Neoplastic030104 developmental biology030220 oncology & carcinogenesisbiology.proteinCancer researchSignal TransductionDevelopmental Biology
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PTEN status is a crucial determinant of the functional outcome of combined MEK and mTOR inhibition in cancer

2017

AbstractCombined MAPK/PI3K pathway inhibition represents an attractive, albeit toxic, therapeutic strategy in oncology. Since PTEN lies at the intersection of these two pathways, we investigated whether PTEN status determines the functional response to combined pathway inhibition. PTEN (gene, mRNA, and protein) status was extensively characterized in a panel of cancer cell lines and combined MEK/mTOR inhibition displayed highly synergistic pharmacologic interactions almost exclusively in PTEN-loss models. Genetic manipulation of PTEN status confirmed a mechanistic role for PTEN in determining the functional outcome of combined pathway blockade. Proteomic analysis showed greater phosphoprote…

0301 basic medicineMAPK/ERK pathwayPTENRNA interferenceprotein Kinase inhibitorsRNA Small InterferinghumansPhosphoinositide-3 Kinase InhibitorsAnimals; cell line tumor; drug synergism; everolimus; female; humans; Janus Kinase 1; MAP Kinase Kinase Kinases; mice; neoplastic stem cells; PTEN phosphohydrolase; phosphatidylinositol 3-Kinases; protein Kinase inhibitors; proto-oncogene Proteins c-akt; Pyridones; Pyrimidinones; RNA Interference; RNA Small Interfering; STAT3 Transcription Factor; TOR Serine-Threonine KinasesMultidisciplinaryMAPK/PI3K pathway inhibitiononcology MAPK/PI3K pathway inhibitionTOR Serine-Threonine Kinasescell lineMAPK/PI3K inhibition oncology. inhibition. PTEN gene mRNA cancer cell lines MEK/mTORMAP Kinase Kinase KinasesfemaleoncologymTORRNA InterferenceSTAT3 Transcription FactortumormicePyridonesMice NudePyrimidinonesBiologyphosphatidylinositol 3-KinasesSmall InterferingArticle03 medical and health sciencesMediatorSettore MED/04 - PATOLOGIA GENERALECell Line TumormedicinePTENAnimalsPI3K/AKT/mTOR pathwaydrug synergismSettore MED/06 - ONCOLOGIA MEDICAneoplastic stem cellsRPTORCancerJanus Kinase 1medicine.diseaseeverolimusproto-oncogene Proteins c-aktBlockade030104 developmental biologyCancer researchbiology.proteinRNAPTEN phosphohydrolase
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Effects of mutations in Wnt/β-catenin, hedgehog, Notch and PI3K pathways on GSK-3 activity—Diverse effects on cell growth, metabolism and cancer

2016

Glycogen synthase kinase-3 (GSK-3) is a serine/threonine kinase that participates in an array of critical cellular processes. GSK-3 was first characterized as an enzyme that phosphorylated and inactivated glycogen synthase. However, subsequent studies have revealed that this moon-lighting protein is involved in numerous signaling pathways that regulate not only metabolism but also have roles in: apoptosis, cell cycle progression, cell renewal, differentiation, embryogenesis, migration, regulation of gene transcription, stem cell biology and survival. In this review, we will discuss the roles that GSK-3 plays in various diseases as well as how this pivotal kinase interacts with multiple sign…

0301 basic medicineMAPK/ERK pathwaySettore MED/06 - Oncologia MedicaCellular differentiationPI3KTargeted therapyGlycogen Synthase Kinase 3Phosphatidylinositol 3-Kinases0302 clinical medicineGSK-3Neoplasmsbeta CateninGSK-3biologyReceptors NotchKinaseWnt signaling pathwayWnt/beta-cateninCell DifferentiationCell biologyGene Expression Regulation Neoplastic030220 oncology & carcinogenesismTORAkt; GSK-3; Hedgehog; Notch; PI3K; Targeted therapy; Therapy resistance; Wnt/beta-catenin; mTORSignal TransductionBeta-cateninNotchAkt GSK-3 Hedgehog mTOR Notch PI3K Targeted therapy Therapy resistance Wnt/beta-cateninCell Survivalmacromolecular substancesNO03 medical and health sciencesAkt; GSK-3 Hedgehog Notch PI3K Targeted therapy Therapy resistance Wnt/beta-catenin mTORAnimalsHumansHedgehog ProteinsProtein kinase BMolecular BiologyPI3K/AKT/mTOR pathwayCell ProliferationAktTherapy resistanceAkt; GSK-3; Hedgehog; mTOR; Notch; PI3K; Targeted therapy; Therapy resistance; Wnt/beta-catenin; Molecular Biology; Cell BiologyCell BiologyWnt ProteinsMicroRNAs030104 developmental biologyMutationCancer researchbiology.proteinTumor Suppressor Protein p53Hedgehog
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Ellagitannin-rich cloudberry inhibits hepatocyte growth factorinduced cell migration and phosphatidylinositol 3-kinase/AKT activation in colon carcin…

2016

// Anne-Maria Pajari 1, 2 , Essi Paivarinta 1 , Lassi Paavolainen 3 , Elina Vaara 1 , Tuuli Koivumaki 4 , Ritu Garg 5 , Anu Heiman-Lindh 1 , Marja Mutanen 1 , Varpu Marjomaki 3 , Anne J. Ridley 2, 5 1 Department of Food and Environmental Sciences, Division of Nutrition, University of Helsinki, Helsinki, Finland 2 University College London, Ludwig Institute for Cancer Research, London, UK 3 Department of Biological and Environmental Science / Nanoscience Center, University of Jyvaskyla, Jyvaskyla, Finland 4 Department of Food and Environmental Sciences, Division of Food Chemistry, University of Helsinki, Helsinki, Finland 5 Randall Division of Cell & Molecular Biophysics, King’s College Lond…

0301 basic medicineMAPK/ERK pathwaycell migrationColorectal cancerCellMetastasisMicePhosphatidylinositol 3-Kinases0302 clinical medicineCell MovementHepatocyte Growth FactorHydrolyzable Tanninsmedicine.anatomical_structureOncology030220 oncology & carcinogenesisColonic NeoplasmsHepatocyte growth factormedicine.drugResearch PapersolumigraatioAntineoplastic Agentscolorectal cancerMet receptorAdenocarcinoma03 medical and health sciencesCell Line TumorellagitanninsmedicineJournal ArticleAnimalsHumansCell migrationProtein kinase Bbusiness.industryPlant Extractsta1182Cancerta3122medicine.diseaseMice Mutant StrainsMin mouseEnzyme ActivationMice Inbred C57BL030104 developmental biologyCancer cellImmunologyCancer researchbusinessRubusProto-Oncogene Proteins c-akt
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BRG1/SMARCA4 is essential for neuroblastoma cell viability through modulation of cell death and survival pathways.

2016

Neuroblastoma (NB) is a neoplasm of the sympathetic nervous system, and is the most common solid tumor of infancy. NBs are very heterogeneous, with a clinical course ranging from spontaneous regression to resistance to all current forms of treatment. High-risk patients need intense chemotherapy, and only 30-40% will be cured. Relapsed or metastatic tumors acquire multi-drug resistance, raising the need for alternative treatments. Owing to the diverse mechanisms that are responsible of NB chemoresistance, we aimed to target epigenetic factors that control multiple pathways to bypass therapy resistance. We found that the SWI/SNF-related, matrix-associated, actin-dependent regulator of chromat…

0301 basic medicineMaleCancer ResearchCombination therapyCell SurvivalBiologyMolecular oncologyTranscriptome03 medical and health sciencesNeuroblastomaPhosphatidylinositol 3-Kinases0302 clinical medicineGrowth factor receptorNeuroblastomaCell Line TumorGeneticsmedicineHumansMolecular BiologyProtein kinase BPI3K/AKT/mTOR pathwayCell ProliferationCell DeathDNA HelicasesNuclear ProteinsCell cyclemedicine.diseaseGene Expression Regulation Neoplastic030104 developmental biologyProto-Oncogene Proteins c-bcl-2030220 oncology & carcinogenesisImmunologyCancer researchFemaleTranscriptomeSignal TransductionTranscription FactorsOncogene
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miRNA92a targets KLF2 and the phosphatase PTEN signaling to promote human T follicular helper precursors in T1D islet autoimmunity.

2016

Aberrant immune activation mediated by T effector cell populations is pivotal in the onset of autoimmunity in type 1 diabetes (T1D). T follicular helper (TFH) cells are essential in the induction of high-affinity antibodies, and their precursor memory compartment circulates in the blood. The role of TFH precursors in the onset of islet autoimmunity and signaling pathways regulating their differentiation is incompletely understood. Here, we provide direct evidence that during onset of islet autoimmunity, the insulin-specific target T-cell population is enriched with a C-X-C chemokine receptor type 5 (CXCR5)(+)CD4(+) TFH precursor phenotype. During onset of islet autoimmunity, the frequency o…

0301 basic medicineMaleReceptors CXCR5endocrine systemAdolescentPopulationPrimary Cell CultureKruppel-Like Transcription FactorsAutoimmunityMice TransgenicNodBiologymedicine.disease_causeCXCR5Autoimmunity03 medical and health sciencesIslets of LangerhansMicePhosphatidylinositol 3-Kinases0302 clinical medicineMice Inbred NODmedicineAnimalsHumansIL-2 receptorKlf2 ; Pten-pi3k Signaling ; T Follicular Helper Cells ; Mirna92a ; Type 1 DiabeteseducationChildPI3K/AKT/mTOR pathwayNOD miceAutoantibodiesgeographyeducation.field_of_studyMultidisciplinarygeography.geographical_feature_categoryForkhead Box Protein O1PTEN PhosphohydrolaseAntagomirsT-Lymphocytes Helper-InducerIsletMicroRNAs030104 developmental biologyDiabetes Mellitus Type 1Gene Expression RegulationImmunologyCancer researchFemale030215 immunologySignal Transduction
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Revisiting the Warburg effect: historical dogma versus current understanding

2020

Contrary to Warburg's original thesis, accelerated aerobic glycolysis is not a primary, permanent and universal consequence of dysfunctional or impaired mitochondria compensating for poor ATP yield per mole of glucose. Instead, in most tumours the Warburg effect is an essential part of a 'selfish' metabolic reprogramming, which results from the interplay between (normoxic/hypoxic) hypoxia-inducible factor-1 (HIF-1) overexpression, oncogene activation (cMyc, Ras), loss of function of tumour suppressors (mutant p53, mutant phosphatase and tensin homologue (PTEN), microRNAs and sirtuins with suppressor functions), activated (PI3K-Akt-mTORC1, Ras-Raf-MEK-ERK-cMyc, Jak-Stat3) or deactivated (LKB…

0301 basic medicineMitochondrial ROSPhysiologyCellular respirationChemistryMitochondrionWarburg effectCell biologyddc:Citric acid cycle03 medical and health sciencesPhosphatidylinositol 3-Kinases030104 developmental biology0302 clinical medicineGlucoseMitochondrial biogenesisAnaerobic glycolysisNeoplasmsTumor MicroenvironmentHumansGlycolysisGlycolysis030217 neurology & neurosurgery
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Triple-negative breast lobular carcinoma: a luminal androgen receptor carcinoma with specific ESRRA mutations.

2021

Primary triple-negative invasive lobular breast carcinomas (TN-ILCs), which do not express hormone receptors and HER2 at diagnosis, are rare and poorly known. In this study, we analyzed the largest TN-ILC series ever reported in the literature, in comparison to phenotypically similar breast tumor subtypes: triple-negative invasive ductal carcinoma (TN-IDC) and hormone receptor-positive invasive lobular carcinoma (HR + ILC). All primary TN-ILCs registered in our database between 2000 and 2018 (n = 38) were compared to tumors from control groups, matched by stage and Elston/Ellis grade, with regard to clinical, pathologic, and immunohistochemical characteristics. A comparative molecular analy…

0301 basic medicineOncologyAdultmedicine.medical_specialtyPathologyReceptor ErbB-2Lobular carcinomaDNA Mutational AnalysisTriple Negative Breast NeoplasmsArticlePathology and Forensic Medicine03 medical and health sciencesBasal (phylogenetics)Phosphatidylinositol 3-Kinases0302 clinical medicineBreast cancerInternal medicinemedicineCarcinomaHumansskin and connective tissue diseasesSurvival analysisAgedAged 80 and overbusiness.industryMiddle Agedmedicine.diseaseAndrogen receptorbody regionsCarcinoma Lobular030104 developmental biologyPleomorphism (cytology)Receptors EstrogenReceptors Androgen030220 oncology & carcinogenesisInvasive lobular carcinomaMutationFemalebusinessModern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
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Molecular alterations in lesions of anogenital mammary-like glands and their mammary counterparts including hidradenoma papilliferum, intraductal pap…

2017

Lesions affecting anogenital mammary-like glands (AGMLG) are histopathologically very similar to those seen in the breast but whether this morphological similarity is also reflected at the genetic level is unknown. To compare the underlying molecular mechanisms in lesions of AGMLG and their mammary counterparts, we analyzed the mutational profile of 16 anogenital neoplasms including 5 hidradenomas papilliferum (HP), 1 lesion with features of HP and fibroadenoma (FA), 7 FA, 3 phyllodes tumors (PhT)) and 18 analogous breast lesions (6 intraductal papillomas (IDP), 9 FA, and 3 PhT) by high-coverage next generation sequencing (NGS) using a panel comprising 50 cancer-related genes. Additionally,…

0301 basic medicinePathologymedicine.medical_specialtyHidradenomaClass I Phosphatidylinositol 3-KinasesBreast NeoplasmsBiologyPathology and Forensic MedicineVulvaMED12Papilloma IntraductalLesionPhosphatidylinositol 3-Kinases03 medical and health sciencessymbols.namesake0302 clinical medicinePhyllodes TumorIntraductal papillomamedicineHumansBreastAgedSanger sequencingVulvar NeoplasmsHigh-Throughput Nucleotide SequencingPhyllodes tumorGeneral MedicineMiddle Agedmedicine.diseaseFibroadenomaTubular Sweat Gland Adenomas030104 developmental biologymedicine.anatomical_structureFibroadenoma030220 oncology & carcinogenesisMutationsymbolsFemalemedicine.symptomAnnals of Diagnostic Pathology
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Cryptotanshinone deregulates unfolded protein response and eukaryotic initiation factor signaling in acute lymphoblastic leukemia cells.

2015

Abstract Background: Unfolded protein responses (UPR) determine cell fate and are recognized as anticancer targets. In a previous research, we reported that cryptotanshinone (CPT) exerted cytotoxic effects toward acute lymphoblastic leukemia cells through mitochondria-mediated apoptosis. Purpose: In the present study, we further investigated the role of UPR in CPT-induced cytotoxicity on acute lymphoblastic leukemia cells by applying tools of pharmacogenomics and bioinformatics. Methods: Gene expression profiling was performed by mRNA microarray hybridization. Potential transcription factor binding motifs were identified in the promoter regions of the deregulated genes by Cistrome software.…

0301 basic medicineendocrine systemXBP1Eukaryotic Initiation Factor-2Pharmaceutical ScienceApoptosisBiology03 medical and health sciencesPhosphatidylinositol 3-KinasesEukaryotic initiation factorCell Line TumorDrug DiscoveryHumansheterocyclic compoundsRNA MessengerEukaryotic Initiation FactorsTranscription factorPharmacologyeIF2ATF4Computational BiologyPromoterPhenanthrenesPrecursor Cell Lymphoblastic Leukemia-LymphomaMolecular Docking Simulation030104 developmental biologyComplementary and alternative medicineCistromePharmacogeneticsEukaryotic Initiation Factor-4AUnfolded protein responseCancer researchUnfolded Protein ResponseMolecular MedicineTranscription Factor CHOPSignal TransductionTranscription FactorsPhytomedicine : international journal of phytotherapy and phytopharmacology
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