Search results for "Phosphoinositide-3 Kinase Inhibitors"

showing 10 items of 22 documents

Targeting chemoresistant colorectal cancer via systemic administration of a BMP7 variant

2020

Abstract Despite intense research and clinical efforts, patients affected by advanced colorectal cancer (CRC) have still a poor prognosis. The discovery of colorectal (CR) cancer stem cell (CSC) as the cell compartment responsible for tumor initiation and propagation may provide new opportunities for the development of new therapeutic strategies. Given the reduced sensitivity of CR-CSCs to chemotherapy and the ability of bone morphogenetic proteins (BMP) to promote colonic stem cell differentiation, we aimed to investigate whether an enhanced variant of BMP7 (BMP7v) could sensitize to chemotherapy-resistant CRC cells and tumors. Thirty-five primary human cultures enriched in CR-CSCs, includ…

0301 basic medicineCancer ResearchColorectal cancerBone Morphogenetic Protein 7Cellular differentiationCellAntineoplastic AgentsTumor initiationBiologyArticleMice03 medical and health sciences0302 clinical medicineSettore MED/04 - PATOLOGIA GENERALECancer stem cellCell Line TumorGeneticsmedicineAnimalsHumansbmp7Molecular BiologyPI3K/AKT/mTOR pathwayPhosphoinositide-3 Kinase InhibitorsCancer stem cellsMesenchymal stem cellWnt signaling pathwayCell Differentiationmedicine.diseasecolorectal cancer bmp7Colorectal cancerXenograft Model Antitumor Assays030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisMutationNeoplastic Stem CellsCancer researchColorectal NeoplasmsOncogene
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Anticancer potential of novel α,β-unsaturated γ-lactam derivatives targeting the PI3K/AKT signaling pathway.

2021

Abstract Six recently synthesized alkyl (Z)-2-(2-oxopyrrolidin-3-ylidene)acetates were evaluated for their potential as cytotoxic and anticancer agents. All compounds were tested in the ERα positive MCF-7, triple negative MDA-MB-231, and Her2+ SKBR-3 breast cancer cell lines. The most lipophilic derivatives, bearing the 4-isopropylphenyl (2) or 4-tert-butylphenyl (3) group at the γ-lactam nitrogen, proved to be cytotoxic against all the cancer cell lines tested (IC50 values ranging from 18 to 63 μM), exerting their greatest activity in SKBR-3 cells, with IC50 values of 33 and 18 μM, respectively. Biological studies showed that the cytotoxic effects of 2 and 3 are accompanied by apoptotic de…

0301 basic medicineLactamsCell SurvivalAntineoplastic AgentsApoptosisBreast NeoplasmsBiochemistry03 medical and health scienceschemistry.chemical_compoundPI3K/AKT signaling pathwayPhosphatidylinositol 3-Kinases0302 clinical medicinebreast cancerCytotoxic T cellHumansα-methylene-γ-lactamsαβ-unsaturated lactamsCytotoxicityPI3K/AKT/mTOR pathwayPhosphoinositide-3 Kinase InhibitorsPharmacologychemistry.chemical_classificationBiological ProductsMolecular StructureChemistryCell growthAkt/PKB signaling pathwayCell CycleEpithelial Cells030104 developmental biologyEnzymeGene Expression RegulationApoptosis030220 oncology & carcinogenesisCancer researchLactamcytotoxicityFemaleProto-Oncogene Proteins c-aktBiochemical pharmacology
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PI3K inhibition reduces murine and human liver fibrogenesis in precisioncut liver slices

2019

Background: Liver fibrosis results from continuous inflammation and injury. Despite its high prevalence worldwide, no approved antifibrotic therapies exist. Omipalisib is a selective inhibitor of the PI3K/mTOR pathway that controls nutrient metabolism, growth and proliferation. It has shown antifibrotic properties in vitro. While clinical trials for idiopathic pulmonary fibrosis have been initiated, an in-depth preclinical evaluation is lacking. We evaluated omipalisib's effects on fibrogenesis using the ex vivo model of murine and human precision-cut tissue slices (PCTS).Methods: Murine and human liver and jejunum PCTS were incubated with omipalisib up to 10 mu M for 48 h. PI3K pathway act…

0301 basic medicineLiver CirrhosisMalePrecision-cut tissue slicesPROGRESSIONPharmacologyBILIARYBiochemistryPI3KGSK2126458JejunumMicePhosphatidylinositol 3-Kinases0302 clinical medicineAdenosine TriphosphateFibrosisFIBROSIShealth care economics and organizationsPhosphoinositide-3 Kinase InhibitorsSulfonamidesPyridazinesmedicine.anatomical_structureJejunumTARGET030220 oncology & carcinogenesisToxicityQuinolinesPhosphorylationmedicine.symptomATP Binding Cassette Transporter Subfamily BLiver fibrosisEARLY-ONSETInflammation03 medical and health sciencesmedicineAnimalsHumansOmipalisibProtein kinase BPI3K/AKT/mTOR pathwayPharmacologybusiness.industryCUT LIVERmedicine.diseaseMice Inbred C57BLMODEL030104 developmental biologybusinessMATRIXEx vivoBiochemical Pharmacology
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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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PI3K-driven HER2 expression is a potential therapeutic target in colorectal cancer stem cells

2020

ObjectiveCancer stem cells are responsible for tumour spreading and relapse. Human epidermal growth factor receptor 2 (HER2) expression is a negative prognostic factor in colorectal cancer (CRC) and a potential target in tumours carrying the gene amplification. Our aim was to define the expression of HER2 in colorectal cancer stem cells (CR-CSCs) and its possible role as therapeutic target in CRC resistant to anti- epidermal growth factor receptor (EGFR) therapy.DesignA collection of primary sphere cell cultures obtained from 60 CRC specimens was used to generate CR-CSC mouse avatars to preclinically validate therapeutic options. We also made use of the ChIP-seq analysis for transcriptional…

0301 basic medicineReceptor ErbB-2Colorectal cancerCetuximabcolorectal cancermedicine.disease_cause03 medical and health sciencesAntineoplastic Agents Immunological0302 clinical medicineSettore MED/04 - PATOLOGIA GENERALECancer stem cellstem cellsTumor Cells CulturedmedicineAdjuvant therapyAnimalsHumansEpidermal growth factor receptorProtein kinase BPI3K/AKT/mTOR pathwayPhosphoinositide-3 Kinase InhibitorsMitogen-Activated Protein Kinase Kinasesdrug resistancebiologybusiness.industryGastroenterologyTrastuzumabmedicine.diseaseantibody targeted therapy030104 developmental biologyDrug Resistance Neoplasm030220 oncology & carcinogenesisNeoplastic Stem CellsCancer researchbiology.proteinKRASPhosphatidylinositol 3-KinaseStem cellColorectal Neoplasmsbusiness
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CD44v6 is a marker of constitutive and reprogrammed cancer stem cells driving colon cancer metastasis.

2014

SummaryCancer stem cells drive tumor formation and metastasis, but how they acquire metastatic traits is not well understood. Here, we show that all colorectal cancer stem cells (CR-CSCs) express CD44v6, which is required for their migration and generation of metastatic tumors. CD44v6 expression is low in primary tumors but demarcated clonogenic CR-CSC populations. Cytokines hepatocyte growth factor (HGF), osteopontin (OPN), and stromal-derived factor 1α (SDF-1), secreted from tumor associated cells, increase CD44v6 expression in CR-CSCs by activating the Wnt/β-catenin pathway, which promotes migration and metastasis. CD44v6− progenitor cells do not give rise to metastatic lesions but, when…

CA15-3Animals; Biomarkers Tumor; Bone Morphogenetic Proteins; Carcinogenesis; Colonic Neoplasms; Fibroblasts; Humans; Hyaluronan Receptors; Mice SCID; Neoplasm Metastasis; Neoplasm Proteins; Neoplastic Stem Cells; Phosphatidylinositol 3-Kinases; Prognosis; Protein Kinase Inhibitors; Proto-Oncogene Proteins c-met; Signal Transduction; Treatment Outcome; Wnt Proteins; Cellular Reprogramming; Molecular Medicine; Genetics; Cell BiologyCarcinogenesisWnt ProteinMice SCIDmedicine.disease_causeAnimals; Antigens CD44; Biomarkers Tumor; Bone Morphogenetic Proteins; Carcinogenesis; Colonic Neoplasms; Fibroblasts; Humans; Mice SCID; Neoplasm Metastasis; Neoplasm Proteins; Neoplastic Stem Cells; Phosphatidylinositol 3-Kinases; Prognosis; Protein Kinase Inhibitors; Proto-Oncogene Proteins c-met; Signal Transduction; Treatment Outcome; Wnt Proteins; Cellular ReprogrammingMetastasisMicePhosphatidylinositol 3-KinasesCD44Neoplasm MetastasisCarcinogenesiPhosphoinositide-3 Kinase InhibitorsColonic NeoplasmTumorbiologyProto-Oncogene Proteins c-metCellular ReprogrammingPrognosisAntigens CD44Neoplasm ProteinsNeoplasm MetastasiAnimals; Antigens CD44; Biomarkers Tumor; Bone Morphogenetic Proteins; Carcinogenesis; Colonic Neoplasms; Fibroblasts; Humans; Mice SCID; Neoplasm Metastasis; Neoplasm Proteins; Neoplastic Stem Cells; Phosphatidylinositol 3-Kinases; Prognosis; Protein Kinase Inhibitors; Proto-Oncogene Proteins c-met; Signal Transduction; Treatment Outcome; Wnt Proteins; Cellular Reprogramming; Cell Biology; Molecular Medicine; GeneticsHyaluronan ReceptorsTreatment OutcomeBone Morphogenetic ProteinsColonic NeoplasmsNeoplastic Stem CellsFibroblastMolecular MedicineHepatocyte growth factorStem cellHumanmedicine.drugSignal TransductionPrognosiProtein Kinase InhibitorSCIDNeoplasm ProteinCancer stem cellSettore MED/04 - PATOLOGIA GENERALEmedicineGeneticsBiomarkers TumorAnimalsHumansAntigensProgenitor cellProtein Kinase InhibitorsSettore MED/04 - Patologia GeneraleAnimalBone Morphogenetic Proteincancer metastasisCD44Cell BiologyFibroblastsmedicine.diseaseWnt ProteinsSettore MED/18 - Chirurgia GeneraleImmunologyCancer researchbiology.proteinNeoplastic Stem CellPhosphatidylinositol 3-KinaseCarcinogenesisBiomarkersCell stem cell
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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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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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HER2 regulates the mammary stem/progenitor cell population driving tumorigenesis and invasion.

2008

The cancer stem cell hypothesis proposes that cancers arise in stem/progenitor cells through disregulation of self-renewal pathways generating tumors, which are driven by a component of 'tumor-initiating cells' retaining stem cell properties. The HER2 gene is amplified in 20-30% of human breast cancers and has been implicated in mammary tumorigenesis as well as in mediating aggressive tumor growth and metastasis. We demonstrate that HER2 overexpression drives mammary carcinogenesis, tumor growth and invasion through its effects on normal and malignant mammary stem cells. HER2 overexpression in normal mammary epithelial cells (NMEC) increases the proportion of stem/progenitor cells as demons…

Cancer ResearchReceptor ErbB-2Cellular differentiationStem cell factorBreast NeoplasmsMice SCIDBiologyStem cell markerAntibodies Monoclonal HumanizedArticleMicePhosphatidylinositol 3-KinasesCancer stem cellMice Inbred NODCell Line TumorGeneticsAnimalsHumansNeoplasm InvasivenessBreastProgenitor cellskin and connective tissue diseasesMolecular BiologyCell ProliferationPhosphoinositide-3 Kinase InhibitorsSettore MED/04 - Patologia GeneraleAntibodies MonoclonalAldehyde DehydrogenaseTrastuzumabEndothelial stem cellImmunologyHER2 Breast Cancer Stem CellsCancer researchNeoplastic Stem CellsFemaleStem cellProto-Oncogene Proteins c-aktAdult stem cellSignal TransductionOncogene
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Aspidin PB, a phloroglucinol derivative, induces apoptosis in human hepatocarcinoma HepG2 cells by modulating PI3K/Akt/GSK3β pathway.

2012

Aspidin PB, a phloroglucinol derivative isolated from Dryopteris fragrans (L.) Schott, has been previously reported to exert high biological activities. In the present study, we analyzed the apoptotic mechanisms of aspidin PB on human hepatoma cell line, HepG2. Initially, aspidin PB was shown to inhibit the growth of HepG2 cells in a time and dose-dependent manner. After treatment with aspidin PB for 72 h, 48 h and 24 h using MTT assay, the IC(50) values were 10.59 μM, 20.86 μM and 46.59 μM, respectively. Aspidin PB was capable to induce apoptosis, as measured by mitochondrial membrane potential (ΔΨm), acridine orange (AO) staining and propidium iodide (PI)/annexin V-FITC double staining. T…

Carcinoma HepatocellularApoptosisBiologyPhloroglucinolToxicologyWortmanninchemistry.chemical_compoundGlycogen Synthase Kinase 3Phosphatidylinositol 3-KinasesAnnexinHumansMTT assayPropidium iodideProtein kinase BProtein Kinase InhibitorsPI3K/AKT/mTOR pathwayCell ProliferationPhosphoinositide-3 Kinase InhibitorsMembrane Potential MitochondrialGlycogen Synthase Kinase 3 betaMicroscopy ConfocalAcridine orangeLiver NeoplasmsGeneral MedicineHep G2 CellsFlow CytometryMolecular biologyAndrostadieneschemistryApoptosisWortmanninProto-Oncogene Proteins c-aktSignal TransductionChemico-biological interactions
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