Search results for " PTEN"

showing 10 items of 10 documents

CeRNA bioinformatic analysis on human telomerase

2013

Messenger RNA (mRNA) translation efficiency is regulated by microRNAs. Each microRNA is able to regulate the translation of multiple mRNAs and each mRNA is regulated by multiple microRNAs. Thus, cellular mRNAs pool competed for microRNAs pool and viceversa. The regulatory network between mRNAs and microRNAs can be studied in the perspective of Competing Endogenous RNAs or ceRNAs. Here it is presented a bioinformatic study on ceRNAs for human telomerase (hTERT). Several genes potentially involved in the regulatory network of hTERT have been harvested by this study. hTERT is essential for the telomeres integrity. Telomere dysfunctions have been widely reported to be involved in Ageing, Cancer…

Settore BIO/18 - GeneticahTERT telomerase PTEN dynein ceRNASettore BIO/11 - Biologia MolecolareSettore MED/13 - Endocrinologia
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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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Transcription factor NRF2 as a therapeutic target for chronic diseases: a systems medicine approach

2018

Systems medicine has a mechanism-based rather than a symptom- or organ-based approach to disease and identifies therapeutic targets in a nonhypothesis-driven manner. In this work, we apply this to transcription factor nuclear factor (erythroid-derived 2)-like 2 (NRF2) by cross-validating its position in a protein-protein interaction network (the NRF2 interactome) functionally linked to cytoprotection in low-grade stress, chronic inflammation, metabolic alterations, and reactive oxygen species formation. Multiscale network analysis of these molecular profiles suggests alterations of NRF2 expression and activity as a common mechanism in a subnetwork of diseases (the NRF2 diseasome). This netw…

0301 basic medicineRMSystems AnalysisNF-E2-Related Factor 2MedicinaNF-KAPPA-BAnti-Inflammatory AgentsTYPE-2 DIABETES-MELLITUSGENE PROMOTER POLYMORPHISMDiseaseComputational biologyInteractomeenvironment and public healthGLYCOGEN-SYNTHASE KINASETUMOR-SUPPRESSOR PTENNRF203 medical and health sciencesDrug DiscoveryAnimalsHumansTherapeutic targetsMedicineMolecular Targeted TherapyBardoxolone methylPLACEBO-CONTROLLED PHASE-3PharmacologyMechanism (biology)Drug discoverybusiness.industryDrug RepositioningRChronic inflammationrespiratory systemHEME OXYGENASE 1PROTEIN-PROTEIN INTERACTION3. Good healthSystems medicineDrug repositioning030104 developmental biologyDrug developmentEXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITISChronic DiseaseSystems medicineMolecular MedicineFUMARIC-ACID ESTERSbusiness
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A Stat6/Pten Axis Links Regulatory T Cells with Adipose Tissue Function

2017

Obesity and type 2 diabetes are associated with metabolic defects and adipose tissue inflammation. Foxp3(+) regulatory T cells (Tregs) control tissue homeostasis by counteracting local inflammation. However, if and how T cells interlink environmental influences with adipocyte function remains unknown. Here, we report that enhancing sympathetic tone by cold exposure, beta3-adrenergic receptor (ADRB3) stimulation or a short-term high-calorie diet enhances Treg induction in vitro and in vivo. CD4(+) T cell proteomes revealed higher expression of Foxp3 regulatory networks in response to cold or ADRB3 stimulation in vivo reflecting Treg induction. Specifically, Ragulator-interacting protein C17o…

0301 basic medicinePTENProteomePhysiologyAdipose tissueStimulationmTORC1Diet induced thermogenesisBorcs6 ; C17orf59 ; Foxp3 ; Pten ; Stat6 ; T Cells ; Tregs ; Adipose Tissue Function ; Cold Exposure ; Metabolic Function ; Metabolism ; Regulatory T cellsT-Lymphocytes Regulatorychemistry.chemical_compound0302 clinical medicineAdipose Tissue BrownAdipocyteUncoupling Protein 1Tissue homeostasisSTAT6ddc:616Mice Inbred BALB CFOXP3Forkhead Transcription Factorshemic and immune systemsRegulatory T cellsCell biologyCold TemperatureFoxp3FemaleMetabolic functionmedicine.symptomSignal TransductionBorcs6Adipose Tissue WhiteCold exposureT cellsTregschemical and pharmacologic phenomenaInflammationBiologyArticle03 medical and health sciencesReceptors Adrenergic betaAdipose tissue functionmedicineAnimalsC17orf59Molecular BiologyPTEN PhosphohydrolaseCell BiologyMetabolism030104 developmental biologychemistryImmunologySTAT6 Transcription Factor030217 neurology & neurosurgeryCell Metabolism
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Targeting the Cancer Initiating Cell: The Ultimate Target for Cancer Therapy

2012

An area of therapeutic interest in cancer biology and treatment is targeting the cancer stem cell, more appropriately referred to as the cancer initiating cell (CIC). CICs comprise a subset of hierarchically organized, rare cancer cells with the ability to initiate cancer in xenografts in genetically modified murine models. CICs are thought to be responsible for tumor onset, self-renewal/maintenance, mutation accumulation and metastasis. CICs may lay dormant after various cancer therapies which eliminate the more rapidly proliferating bulk cancer (BC) mass. However, CICs may remerge after therapy is discontinued as they may represent cells which were either intrinsically resistant to the or…

PTENgerminal mutationchemotherapeuticmedicine.medical_treatmentAntineoplastic AgentsPI3KTargeted therapyMetastasisMice03 medical and health sciencesTARGETED THERAPY0302 clinical medicineCancer stem cellNeoplasmsradiologicalDrug DiscoverymedicineAnimalsHumansPTENAkt; mTOR; PI3K; PTEN; Targeted therapy; Therapeutic sensitivityPI3K/AKT/mTOR pathway030304 developmental biologyPharmacologyBiological Products0303 health sciencesbiologyAKTMTORAktCD44Wnt signaling pathwayCancertargeted therapymedicine.disease3. Good healththerapeutic sensitivityxenografts030220 oncology & carcinogenesisImmunologymTORNeoplastic Stem CellsCancer researchbiology.proteinCurrent Pharmaceutical Design
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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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PTEN hamartoma tumor syndromes in childhood: description of two cases and a proposal for follow-up protocol

2013

PTEN hamartoma tumor syndromes (PHTS) are a spectrum of hamartomatous overgrowth syndromes associated with germ-line mutations in the tumor suppressor PTEN gene located on 10q23.3. It is widely accepted that two of these disorders, Cowden syndrome and Bannayan-Riley-Ruvalcaba syndrome, are allelic conditions. Because PTEN mutations are not identifiable in every case of the PHTS phenotype, the inability to detect a mutation within the PTEN gene does not invalidate the clinical diagnosis of Cowden syndrome, or Bannayan-Riley-Ruvalcaba syndrome, in patients who meet diagnostic criteria for these disorders. PTEN mutations are associated with an increased risk for developing breast, thyroid, end…

OncologyPTENmedicine.medical_specialtymedicine.disease_causeBannayan–Riley–Ruvalcaba syndromeSettore MED/38 - Pediatria Generale E SpecialisticaInternal medicineGeneticsmedicinePTEN Hamartoma tumor syndromeHamartomaPTENAllelePTEN Hamartoma tumor syndromes; PTEN gene; Cowden syndrome; Bannayan-Riley-Ruvalcaba syndromGenetics (clinical)Bannayan-Riley-Ruvalcaba syndromMutationbiologybusiness.industryThyroidCancerCowden syndromeCowden syndromePTEN genemedicine.diseasemedicine.anatomical_structureSettore MED/31 - OtorinolaringoiatriaSettore MED/03 - Genetica Medicabiology.proteinCancer researchbusiness
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Sirolimus treatment of severe PTEN hamartoma tumor syndrome: case report and in vitro studies

2013

Background: Phosphatase and tensin homolog (PTEN) hamartoma tumor syndrome (PHTS) is caused by germ line mutations in the PTEN gene. Symptoms include cancer pre- disposition, immune deviations, and lipomas/lipomatosis. No causal standard therapy is available. We describe a therapeutic attempt with the mammalian target of rapamycin (mTOR) inhibitor sirolimus for a PHTS patient suffering from thymus hyperplasia and lipomatosis. We furthermore assessed the in vitro effects of sirolimus and other inhibitors on lipoma cells of the patient. Methods: The patient underwent clinical and blood examinations and whole-body magnetic resonance imaging to assess tumor sizes. Lipoma cells of the patient we…

LipomatosisIn Vitro TechniquesDrug therapy Hamartoma Paediatrics PTEN PHTS PI3K AKT mTORmedicineHumansTensinPTENddc:610Protein kinase BPI3K/AKT/mTOR pathwaySirolimusbiologybusiness.industryInfant NewbornPTEN PhosphohydrolaseInfantLipomamedicine.diseaseChild PreschoolSirolimusPediatrics Perinatology and Child HealthCancer researchbiology.proteinThymus hyperplasiaHamartoma Syndrome Multiplebusinessmedicine.drugPediatric Research
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In human retinoblastoma Y79 cells okadaic acid-parthenolide co-treatment induces synergistic apoptotic effects, with PTEN as a key player.

2013

Retinoblastoma is the most common intraocular malignancy of childhood. In developing countries, treatment is limited, long-term survival rates are low and current chemotherapy causes significant morbidity to pediatric patients and significantly limits dosing. Therefore there is an urgent need to identify new therapeutic strategies to improve the clinical outcome of patients with retinoblastoma. here, we investigated the effects of two natural compounds okadaic acid (OKa) and parthenolide (PN) on human retinoblastoma Y79 cells. For the first time we showed that OKa/PN combination at subtoxic doses induces potent synergistic apoptotic effects accompanied by lowering in p-akt levels, increasin…

Cancer ResearchCell SurvivalGene ExpressionAntineoplastic AgentsApoptosisBiologychemistry.chemical_compoundSettore BIO/10 - BiochimicaCell Line TumorOkadaic AcidmedicinePTENCytotoxic T cellHumansParthenolideViability assayProtein kinase BCell ShapePharmacologyRetinoblastomaPTEN PhosphohydrolaseRetinoblastomaDrug SynergismProto-Oncogene Proteins c-mdm2Okadaic acidmedicine.diseaseGlutathioneOxidative StressOncologychemistryApoptosisCancer researchbiology.proteinMolecular Medicineretinoblastoma Y79 cells synergistic apoptotic effects oxidative stress natural drugs PTEN/Akt/Mdm2/p53 pathway parthenolide okadaic acid.Drug Screening Assays AntitumorTumor Suppressor Protein p53Reactive Oxygen SpeciesProtein Processing Post-TranslationalProto-Oncogene Proteins c-aktSesquiterpenesResearch PaperCancer biologytherapy
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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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