Search results for "Oncogene protein"

showing 10 items of 812 documents

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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Expression of WISPs and of their novel alternative variants in human hepatocellular carcinoma cells

2005

WISPs (Wnt-induced secreted proteins) are members of the CCN (CTGF/Cyr61/Nov) family involved in fibrotic disorders and tumorigenesis. They have a typical structure composed of four conserved cysteine-rich modular domains, but variants of CCN members lacking one or more modules, generated by alternative splicing or gene mutations, have been described in various pathological conditions. WISP genes were first described as downstream targets of the Wnt signaling pathway, which is frequently altered in human hepatocellular carcinoma (HCC). In the present study, WISP mRNA expression was analyzed by RT-PCR in four human HCC cell lines (HepG2, HuH-6, HuH-7, HA22T/VGH). Our results show for the fir…

Carcinoma HepatocellularWISPHepatocellular carcinomaApoptosisGene mutationBiologymedicine.disease_causeGeneral Biochemistry Genetics and Molecular BiologyCCN Intercellular Signaling ProteinsWntalternative splicingHistory and Philosophy of ScienceCell Line TumorProto-Oncogene ProteinsCCN Intercellular Signaling ProteinsmedicineHumansRNA MessengerGeneDNA PrimersOncogene ProteinsGeneticsCCNModels GeneticReverse Transcriptase Polymerase Chain ReactionGeneral NeuroscienceLiver NeoplasmsAlternative splicingIntracellular Signaling Peptides and ProteinsWnt signaling pathwaydigestive system diseasesNeoplasm ProteinsInsulin-Like Growth Factor Binding ProteinsRepressor ProteinsCTGFCYR61Cancer researchIntercellular Signaling Peptides and ProteinsRNACarcinogenesisWISPWntTranscription Factors
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Oligodendroglial p130Cas Is a Target of Fyn Kinase Involved in Process Formation, Cell Migration and Survival

2014

Oligodendrocytes are the myelinating glial cells of the central nervous system. In the course of brain development, oligodendrocyte precursor cells migrate, scan the environment and differentiate into mature oligodendrocytes with multiple cellular processes which recognize and ensheath neuronal axons. During differentiation, oligodendrocytes undergo dramatic morphological changes requiring cytoskeletal rearrangements which need to be tightly regulated. The non-receptor tyrosine kinase Fyn plays a central role in oligodendrocyte differentiation and myelination. In order to improve our understanding of the role of oligodendroglial Fyn kinase, we have identified Fyn targets in these cells. Pur…

Cell Survival610 Medizinlcsh:MedicineProto-Oncogene Proteins c-fynSignaling PathwaysMiceCell Movement610 Medical sciencesMolecular Cell BiologyAnimalsPhosphorylationlcsh:ScienceBiologyCells CulturedNeuronslcsh:RCell DifferentiationMolecular DevelopmentSignalingAxonsOligodendrogliaCrk-Associated Substrate ProteinCellular Neurosciencelcsh:QCellular TypesMolecular NeuroscienceResearch ArticleDevelopmental BiologyNeurosciencePLoS ONE
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Quinoline-Based Molecules Targeting c-Met, EGF, and VEGF Receptors and the Proteins Involved in Related Carcinogenic Pathways

2020

The quinoline ring system has long been known as a versatile nucleus in the design and synthesis of biologically active compounds. Currently, more than one hundred quinoline compounds have been approved in therapy as antimicrobial, local anaesthetic, antipsychotic, and anticancer drugs. In drug discovery, indeed, over the last few years, an increase in the publication of papers and patents about quinoline derivatives possessing antiproliferative properties has been observed. This trend can be justified by the versatility and accessibility of the quinoline scaffold, from which new derivatives can be easily designed and synthesized. Within the numerous quinoline small molecules developed as a…

Cell SurvivalAngiogenesisPharmaceutical ScienceAntineoplastic AgentsReviewMolecular Dynamics SimulationAnalytical Chemistrylcsh:QD241-441Structure-Activity Relationship03 medical and health scienceschemistry.chemical_compound0302 clinical medicinelcsh:Organic chemistryEpidermal growth factorquinolineDrug DiscoverySAR studieHumansPhysical and Theoretical Chemistrycarcinogenic pathwaysProtein kinase BPI3K/AKT/mTOR pathway030304 developmental biology0303 health sciencesantiproliferative compoundChemistryDrug discoveryOrganic ChemistryQuinolineBiological activityProto-Oncogene Proteins c-metantiproliferative compoundstargeted therapySettore CHIM/08 - Chimica FarmaceuticaSmall moleculeErbB Receptorscarcinogenic pathwayReceptors Vascular Endothelial Growth FactorSAR studiesChemistry (miscellaneous)030220 oncology & carcinogenesisQuinolinesCancer researchMolecular Medicinekinases modulatorkinases modulatorsbiological dataSignal TransductionMolecules
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Induction of programmed cell death in human retinoblastoma Y79 cells by C2-ceramide.

1998

C2-ceramide, a cell-permeable analogue of ceramide, induced significant, dose- and time-dependent death in human retinoblastoma Y79 cells. Dying cells strongly displayed the morphology of apoptosis as characterized by microscopic evidence of cell shrinkage, membrane blebbing, nuclear and chromatin condensation and degeneration of the nucleus into membrane-bound apoptotic bodies. Upon induction of apoptosis Y79 cells evidence early phosphatidylserine externalization, as shown by annexin V-FITC. Apoptosis was also assessed by monitoring changes in cell granularity by staining with the combined fluorescent dyes acridine orange and ethidium bromide. C2-ceramide induced these morphological chang…

Cell SurvivalBlotting WesternRetinoblastomaProteinsApoptosisDNA FragmentationCeramidesC2-ceramideNucleosomesSphingomyelin PhosphodiesteraseBacterial ProteinsProto-Oncogene Proteins c-bcl-2SphingosineOkadaic AcidTumor Cells CulturedHumansTumor Suppressor Protein p53Interleukin-1Molecular and cellular biochemistry
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Differential regulation of apoptosis-associated genes by estrogen receptor alpha in human neuroblastoma cells

2012

Purpose: The neuroendocrinology of female sex hormones is of great interest for a variety of neuropsychiatric disorders. In fact, estrogens and estrogen receptors (ERs) exert neuromodulatory and neuroprotective functions. Here we investigated potential targets of the ER subtype alpha that may mediate neuroprotection and focused on direct modulators and downstream executors of apoptosis. Methods: We employed subclones of human neuroblastoma cells (SK-N-MC) stably transfected with one of the ER subtypes, ERalpha or ERbeta. Differences between the cell lines regarding the mRNA expression levels were examined by qPCR, changes on protein levels were examined by Western Blot and immunocytochemist…

Cell SurvivalEstrogen receptorApoptosisCaspase 3BiologyNeuroprotectionRats Sprague-DawleyNeuroblastomaDevelopmental NeuroscienceCell Line TumorAnimalsEstrogen Receptor betaHumansGene silencingAdaptor Proteins Signal TransducingNeuronsCaspase 3Estrogen Receptor alphaTransfectionMolecular biologyRatsUp-RegulationDNA-Binding ProteinsProto-Oncogene Proteins c-bcl-2NeurologyCell cultureApoptosisCancer researchNeurology (clinical)Apoptosis Regulatory ProteinsEstrogen receptor alphahormones hormone substitutes and hormone antagonistsTranscription FactorsRestorative Neurology and Neuroscience
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NKG2D induces Mcl-1 expression and mediates survival of CD8 memory T cell precursors via phosphatidylinositol 3-kinase.

2013

Abstract Memory formation of activated CD8 T cells is the result of a specific combination of signals that promote long-term survival and inhibit differentiation into effector cells. Much is known about initial cues that drive memory formation, but it is poorly understood which signals are essential during the intermediate stages before terminal differentiation. NKG2D is an activating coreceptor on Ag-experienced CD8 T cells that promotes effector cell functions. Its role in memory formation is currently unknown. In this study, we show that NKG2D controls formation of CD8 memory T cells by promoting survival of precursor cells. We demonstrate that NKG2D enhances IL-15–mediated PI3K signalin…

Cell SurvivalImmunologyCytomegalovirusBiologyCD8-Positive T-LymphocytesLymphocyte ActivationMiceMemory cellPrecursor cellmedicineImmunology and AllergyCytotoxic T cellAnimalsIL-2 receptorReceptors ImmunologicInterleukin-15Mice KnockoutPrecursor Cells T-LymphoidNK cells; NKG2D; CD8 T cellsEffectorCell DifferentiationNKG2DNKG2D; CD8 T cell memory; Mcl1; PI3KCell biologyMice Inbred C57BLmedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2NK Cell Lectin-Like Receptor Subfamily KCytomegalovirus InfectionsMyeloid Cell Leukemia Sequence 1 ProteinPhosphatidylinositol 3-KinaseMemory T cellImmunologic MemoryCD8Signal TransductionJournal of immunology (Baltimore, Md. : 1950)
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Cell cycle arrest and induction of apoptosis by cajanin stilbene acid from Cajanus cajan in breast cancer cells

2015

Abstract Background: The low abundant cajanin stilbene acid (CSA) from Pigeon Pea ( Cajanus cajan ) has been shown to kill estrogen receptor α positive cancer cells in vitro and in vivo . Downstream effects such as cell cycle and apoptosis-related mechanisms have not been analyzed yet. Material and methods: We analyzed the activity of CSA by means of flow cytometry (cell cycle distribution, mitochondrial membrane potential, MMP), confocal laser scanning microscopy (MMP), DNA fragmentation assay (apoptosis), Western blotting (Bax and Bcl-2 expression, caspase-3 activation) as well as mRNA microarray hybridization and Ingenuity pathway analysis. Results: CSA induced G2/M arrest and apoptosis …

Cell cycle checkpointDNA damageCellPharmaceutical ScienceApoptosisBiologyFlow cytometryCajanusStilbenesDrug DiscoverymedicineHumansbcl-2-Associated X ProteinMembrane Potential MitochondrialPharmacologymedicine.diagnostic_testCaspase 3Cell Cycle CheckpointsCell cycleMolecular biologySalicylatesGene Expression Regulation Neoplasticmedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2Complementary and alternative medicineApoptosisCancer cellMCF-7 CellsMolecular MedicineDNA fragmentationDNA DamageSignal TransductionPhytomedicine
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The MDM2-p53 pathway is involved in preconditioning-induced neuronal tolerance to ischemia

2018

Brain preconditioning (PC) refers to a state of transient tolerance against a lethal insult that can be evoked by a prior mild event. It is thought that PC may induce different pathways responsible for neuroprotection, which may involve the attenuation of cell damage pathways, including the apoptotic cell death. In this context, p53 is a stress sensor that accumulates during brain ischemia leading to neuronal death. The murine double minute 2 gene (MDM2), a p53-specific E3 ubiquitin ligase, is the main cellular antagonist of p53, mediating its degradation by the proteasome. Here, we study the role of MDM2-p53 pathway on PC-induced neuroprotection both in cultured neurons (in vitro) and rat …

Cell death0301 basic medicineProgrammed cell deathCell SurvivalNeuronalScience2415 Biología MolecularIschemiaNeuroprotectionArticleBrain ischemiaMiceBrain ischemia03 medical and health sciences0302 clinical medicineIschemiaXarxes neuronals (Neurobiologia)medicineAnimalsIschemic PreconditioningCell damageCells CulturedBrain preconditioningNeuronsMultidisciplinarybiologyChemistryQRBrainProto-Oncogene Proteins c-mdm2MDM2-p53medicine.diseaseNeuroprotectionRatsCell biologyUbiquitin ligaseDisease Models Animal030104 developmental biology2490 Neurocienciasbiology.proteinMedicineIschemic preconditioningMdm2Tumor Suppressor Protein p53030217 neurology & neurosurgerySignal Transduction
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Differential regulation of the clusterin gene by Ha-ras and c-myc oncogenes and during apoptosis

1998

Clusterin (ApoJ) is an extracellular glycoprotein expressed during processes of tissue differentiation and regression that involve programmed cell death (apoptosis). Increased clusterin expression has also been found in tumors, however, the mechanism underlying this induction is not known. Apoptotic processes in tumors could be responsible for clusterin gene activation. Alternatively, oncogenic mutations could modulate signal transduction, thereby inducing the gene. We examined the response of the rat clusterin gene to two oncogenes, Ha-ras and c-myc, in transfected Rat1 fibroblasts. While c-myc overexpression did not modify clusterin gene activity, the Ha-ras oncogene produced a seven to t…

Cell signalingProgrammed cell deathUltraviolet RaysPhysiologyRecombinant Fusion ProteinsClinical BiochemistryGenes mycApoptosisDNA FragmentationBiologyTransfectionProto-Oncogene Proteins c-mycProto-Oncogene Proteins p21(ras)AnimalsRNA MessengerCell Line TransformedGlycoproteinsOncogeneClusterinCell CycleCell BiologyTransfectionFibroblastsCell cycleeye diseasesRatsClusterinGenes rasApoptosisMutationCancer researchbiology.proteinsense organsSignal transductionMolecular ChaperonesSignal TransductionJournal of Cellular Physiology
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