Search results for "Neoplastic"

showing 10 items of 2901 documents

Targeting heat shock proteins in cancer

2010

Heat shock proteins (HSPs) HSP27, HSP70 and HSP90 are powerful chaperones. Their expression is induced in response to a wide variety of physiological and environmental insults including anti-cancer chemotherapy, thus allowing the cell to survive to lethal conditions. Different functions of HSPs have been described to account for their cytoprotective function, including their role as molecular chaperones as they play a central role in the correct folding of misfolded proteins, but also their anti-apoptotic properties. HSPs are often overexpressed in cancer cells and this constitutive expression is necessary for cancer cells' survival. HSPs may have oncogene-like functions and likewise mediat…

Protein Foldingendocrine systemCancer ResearchCell SurvivalProtein ConformationCellAntineoplastic AgentsApoptosisBreast NeoplasmsHsp27NeoplasmsHeat shock proteinmedicineAnimalsHumansHSP70 Heat-Shock ProteinsHSP90 Heat-Shock ProteinsHeat-Shock ProteinsCell ProliferationbiologyCell growthCancermedicine.diseaseHsp90Hsp70Cell biologymedicine.anatomical_structureOncologyDrug Resistance NeoplasmCancer cellbiology.proteinMolecular ChaperonesCancer Letters
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Peroxisomal and mitochondrial status of two murine oligodendrocytic cell lines (158N, 158JP): potential models for the study of peroxisomal disorders…

2009

International audience; In some neurodegenerative disorders (leukodystrophies) characterized by myelin alterations, the defect of peroxisomal functions on myelin-producing cells (oligodendrocytes) are poorly understood. The development of in vitro models is fundamental to understanding the physiopathogenesis of these diseases. We characterized two immortalized murine oligodendrocyte cell lines: a normal (158N) and a jimpy (158JP) cell line mutated for the proteolipid protein PLP/DM20. Fluorescence microscopy, flow cytometry, and western blotting analysis allow to identify major myelin proteins (PLP colocalizing with mitochondria; myelin basic protein), oligodendrocyte (CNPase and myelin oli…

Proteolipid protein 1BiochemistryMiceMyelinMESH : PhenylbutyratesperoxisomeIsomerasesMESH : Myelin Basic ProteinsEnoyl-CoA HydrataseCell Line TransformedUltrasonographybiologyMESH : Gene Expression RegulationMESH : Myelin Proteolipid Protein3-Hydroxyacyl CoA DehydrogenasesMESH : Myelin-Associated GlycoproteinMESH : Cell Line TransformedPeroxisomeMESH : Multienzyme ComplexesMESH : OligodendrogliaMESH : Enoyl-CoA HydrataseCatalaseFlow CytometryMESH : 3-Hydroxyacyl CoA DehydrogenasesPhenylbutyratesmitochondriaMyelin-Associated GlycoproteinOligodendrogliamyelinMESH : Antineoplastic Agentsmedicine.anatomical_structureMESH : Microscopy Electron TransmissionBiochemistryACOX1MESH : MitochondriaMESH : Acyl-CoA Oxidase2'3'-Cyclic-Nucleotide PhosphodiesterasesMESH : IsomerasesOxidation-ReductionMyelin ProteinsMESH : Flow CytometryAntineoplastic AgentsPeroxisomal Bifunctional EnzymeStatistics NonparametricMyelin oligodendrocyte glycoproteinCellular and Molecular NeuroscienceMicroscopy Electron TransmissionMultienzyme ComplexesMESH : CatalaseMESH : MicePeroxisomesmedicineAnimalsMESH : ATP-Binding Cassette TransportersMyelin Proteolipid ProteinMESH : Statistics Nonparametric[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH : Oxidation-ReductionMyelin Basic Proteinmurine oligodendrocytesMESH : 2'3'-Cyclic-Nucleotide PhosphodiesterasesPeroxisomal transportOligodendrocyteMyelin basic proteinGene Expression Regulationbiology.proteinATP-Binding Cassette TransportersMyelin-Oligodendrocyte GlycoproteinAcyl-CoA OxidaseMESH : AnimalsMESH : Peroxisomes
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Effect of transfection with PLP2 antisense oligonucleotides on gene expression of cadmium-treated MDA-MB231 breast cancer cells

2012

Emerging evidence indicates that cadmium (Cd) is able to regulate gene expression, drastically affecting the pattern of transcriptional activity in human normal and pathological cells. We have already shown that exposure of MDA-MB231 breast cancer cells to 5 μM CdCl(2) for 96 h, apart from significantly affecting mitochondrial metabolism, induces modifications of the expression level of genes coding for members of stress response-, mitochondrial respiration-, MAP kinase-, NF-κB-, and apoptosis-related pathways. In the present study, we have expanded the knowledge on the biological effects of Cd-breast cancer cell interactions, indicating PLP2 (proteolipid protein-2) as a novel member of the…

ProteolipidsApoptosisBreast NeoplasmsTransfectionBiochemistryAnalytical ChemistryCadmium ChlorideStress PhysiologicalCell Line TumorGene expressionHumansRNA MessengerSettore BIO/06 - Anatomia Comparata E Citologiaskin and connective tissue diseasesGeneCaspaseHeat-Shock ProteinsMARVEL Domain-Containing Proteinsbiologycadmium PLP2 breast cancer differential display-PCR caspase gene expressionTransfectionSuicide geneOligonucleotides AntisenseMolecular biologyGene Expression Regulation NeoplasticApoptosisMitogen-activated protein kinaseCaspasesCancer cellbiology.proteinNucleic Acid ConformationFemale
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Proteomic and transcriptomic profiling reveals a link between the PI3K pathway and lower estrogen-receptor (ER) levels and activity in ER+ breast can…

2010

Introduction Accumulating evidence suggests that both levels and activity of the estrogen receptor (ER) and the progesterone receptor (PR) are dramatically influenced by growth-factor receptor (GFR) signaling pathways, and that this crosstalk is a major determinant of both breast cancer progression and response to therapy. The phosphatidylinositol 3-kinase (PI3K) pathway, a key mediator of GFR signaling, is one of the most altered pathways in breast cancer. We thus examined whether deregulated PI3K signaling in luminal ER+ breast tumors is associated with ER level and activity and intrinsic molecular subtype. Methods We defined two independent molecular signatures of the PI3K pathway: a pro…

ProteomeMessengerEstrogen receptorPhosphatidylinositol 3-Kinases0302 clinical medicineReceptorsTumor Cells CulturedInsulin-Like Growth Factor IReceptorCancerOligonucleotide Array Sequence AnalysisMedicine(all)0303 health sciencesCulturedTumorBlottingReverse Transcriptase Polymerase Chain ReactionPrognosis3. Good healthTumor CellsGene Expression Regulation NeoplasticReceptors Estrogen030220 oncology & carcinogenesisFemaleSignal transductionWesternmedicine.drugBiotechnologySignal TransductionResearch Articlemedicine.medical_specialtyBlotting WesternOncology and CarcinogenesisBreast NeoplasmsBiology03 medical and health sciencesInternal medicineProgesterone receptorBreast CancerBiomarkers TumormedicineGeneticsHumansRNA MessengerOncology & CarcinogenesisPI3K/AKT/mTOR pathway030304 developmental biologyCell ProliferationNeoplasticCell growthGene Expression ProfilingEstrogenGene expression profilingEndocrinologyGene Expression RegulationCancer researchRNAProto-Oncogene Proteins c-aktTamoxifenBiomarkersBreast Cancer Research : BCR
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Investigation of cancer drug resistance mechanisms by phosphoproteomics

2020

Abstract Cancer cell mutations can be identified by genomic and transcriptomic techniques. However, they are not sufficient to understand the full complexity of cancer heterogeneity. Analyses of proteins expressed in cancers and their modification profiles show how these mutations could be translated at the functional level. Protein phosphorylation is a major post-translational modification critical for regulating several cellular functions. The covalent addition of phosphate groups to serine, threonine, and tyrosine is catalyzed by protein kinases. Over the past years, kinases were strongly associated with cancer, thus inhibition of protein kinases emanated as novel cancer treatment. Howev…

Proteomics0301 basic medicineProteomeAntineoplastic AgentsBiologyProteomics03 medical and health sciences0302 clinical medicineNeoplasmsBiomarkers TumormedicineAnimalsHumansProtein phosphorylationPhosphorylationProtein Kinase InhibitorsPharmacologyKinasePhosphoproteomicsCancermedicine.diseaseNeoplasm Proteins030104 developmental biologyDrug Resistance Neoplasm030220 oncology & carcinogenesisCancer cellCancer researchPhosphorylationProtein Processing Post-TranslationalTyrosine kinasePharmacological Research
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Proteomic identification of the heterogeneous nuclear ribonucleoprotein K as irradiation responsive protein related to migration

2014

Abstract Irradiation resistance is a major obstacle of head and neck squamous cell carcinoma (HNSCC) therapy, limiting treatment success and patient survival. The aim of our experiments was to identify irradiation-regulated proteins as potential drug targets. Two established HNSCC cell lines (HNSCCUM-01T and HNSCCUM-02T) were treated with a single 8 Gy (Gray) fraction of irradiation. Changes in cellular protein expression were studied after 24 h by means of 2D-electrophoresis and MALDI–TOF-mass spectrometry. Ninety-four differentially expressed proteins were identified. The expression levels of four proteins were regulated similarly in both cell lines after irradiation treatment, i.e., GRP7…

ProteomicsBiophysicsBiologyBiochemistryCellular proteinImmunocytochemical stainingHeterogeneous-Nuclear Ribonucleoprotein KCell MovementCell Line TumormedicineHumansHeterogeneous-Nuclear Ribonucleoprotein KIrradiationNeoplasm MetastasisEndoplasmic Reticulum Chaperone BiPmedicine.diseaseMolecular biologyHead and neck squamous-cell carcinomaNeoplasm ProteinsGene Expression Regulation NeoplasticBlotRibonucleoproteinsGamma RaysHead and Neck NeoplasmsBiological significanceCell cultureCarcinoma Squamous CellCancer researchJournal of Proteomics
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Integrative genomic and proteomic analyses identify targets for Lkb1 deficient metastatic lung tumors

2010

SummaryIn mice, Lkb1 deletion and activation of KrasG12D results in lung tumors with a high penetrance of lymph node and distant metastases. We analyzed these primary and metastatic de novo lung cancers with integrated genomic and proteomic profiles, and have identified gene and phosphoprotein signatures associated with Lkb1 loss and progression to invasive and metastatic lung tumors. These studies revealed that SRC is activated in Lkb1-deficient primary and metastatic lung tumors, and that the combined inhibition of SRC, PI3K, and MEK1/2 resulted in synergistic tumor regression. These studies demonstrate that integrated genomic and proteomic analyses can be used to identify signaling pathw…

ProteomicsCancer ResearchLung NeoplasmsMAP Kinase Kinase 2MAP Kinase Kinase 1CELLCYCLEAMP-Activated Protein Kinasesmedicine.disease_causeMice0302 clinical medicineAMP-Activated Protein Kinase KinasesCell MovementCarcinoma Non-Small-Cell LungEnzyme InhibitorsNeoplasm MetastasisPhosphorylationLymph nodePhosphoinositide-3 Kinase Inhibitors0303 health sciencesTOR Serine-Threonine KinasesIntracellular Signaling Peptides and ProteinsGenomicsCell cycleProtein-Tyrosine KinasesPenetrance3. Good healthUp-RegulationGene Expression Regulation Neoplasticmedicine.anatomical_structuresrc-Family KinasesOncologySIGNALING030220 oncology & carcinogenesisDrug Therapy CombinationFemaleRNA InterferenceKRASSignal TransductionMice NudeBiologyProtein Serine-Threonine KinasesArticleProto-Oncogene Proteins p21(ras)03 medical and health sciencesCell Line TumorProto-Oncogene ProteinsmedicineCell AdhesionAnimalsHumansEpithelial–mesenchymal transitionProtein Kinase Inhibitors030304 developmental biologyFocal AdhesionsGene Expression ProfilingCell BiologyXenograft Model Antitumor AssaysMice Mutant StrainsGene expression profilingFocal Adhesion Protein-Tyrosine KinasesCancer cellCell TransdifferentiationCancer researchras ProteinsCarcinogenesis
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Integrative analysis of cyclin protein levels identifies cyclin b1 as a classifier and predictor of outcomes in breast cancer

2009

Abstract Purpose: We studied the expression levels of cyclins B1, D1, and E1 and the implications of cyclin overexpression for patient outcomes in distinct breast cancer subtypes defined by clinical variables and transcriptional profiling. Experimental Design: The expression levels of cyclins B1, D1, and E1 were quantified in 779 breast tumors and 53 cell lines using reverse phase protein arrays and/or transcriptional profiling. Results: Whereas cyclin E1 overexpression was a specific marker of triple-negative and basal-like tumors, cyclin B1 overexpression occurred in poor prognosis hormone receptor–positive, luminal B and basal-like breast cancers. Cyclin D1 overexpression occurred in lum…

ProteomicsCancer ResearchPathologymedicine.medical_specialtyCyclin EClass I Phosphatidylinositol 3-KinasesCyclin DDNA Mutational AnalysisCyclin BBreast NeoplasmsBiologyCyclin BArticlePhosphatidylinositol 3-KinasesCyclin D1Predictive Value of TestsCell Line TumorCyclin Emedicine1-Phosphatidylinositol 3-KinaseHumansCyclin D1BreastCyclin B1Cyclin B1Oligonucleotide Array Sequence AnalysisProportional Hazards ModelsOncogene ProteinsGene Expression ProfilingCancermedicine.diseasePrognosisImmunohistochemistrySurvival AnalysisGene Expression Regulation NeoplasticCyclin E1OncologyReceptors EstrogenSpectrometry Mass Matrix-Assisted Laser Desorption-IonizationMutationCancer researchbiology.proteinFemaleBreast diseaseReceptors Progesterone
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Role of Extracellular Vesicles in Hematological Malignancies.

2015

In recent years the role of tumor microenvironment in the progression of hematological malignancies has been widely recognized. Recent studies have focused on how cancer cells communicate within the microenvironment. Among several factors (cytokines, growth factors, and ECM molecules), a key role has been attributed to extracellular vesicles (EV), released from different cell types. EV (microvesicles and exosomes) may affect stroma remodeling, host cell functions, and tumor angiogenesis by inducing gene expression modulation in target cells, thus promoting cancer progression and metastasis. Microvesicles and exosomes can be recovered from the blood and other body fluids of cancer patients a…

ProteomicsCell typeImmunology and Microbiology (all)lcsh:MedicineReview ArticleBiologyProteomicsExosomesGeneral Biochemistry Genetics and Molecular BiologyMetastasisExtracellular VesiclesStromaSettore BIO/13 - Biologia ApplicatamedicineTumor MicroenvironmentHumansTumor microenvironmentBiochemistry Genetics and Molecular Biology (all)General Immunology and MicrobiologyNeovascularization Pathologiclcsh:RCancerGeneral Medicinemedicine.diseaseMicrovesiclesCell biologyGene Expression Regulation NeoplasticHematologic NeoplasmsCancer cellBiochemistry Genetics and Molecular Biology (all); Immunology and Microbiology (all)BioMed research international
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Effect of collagen substrates on proteomic modulation of breast cancer cells

2004

We have previously described the occurrence, in breast and colon cancer extra-cellular matrix, of an oncofoetal form of collagen, OF/LB, able to induce an increase in cell proliferation and motility in the breast cancer cell line 8701-BC. It also caused an increased amount of type V collagen which appears to exert an anti-proliferative effect on the same cells. The aim of the present study was to investigate, at the proteomic level, the effect of OF/LB and type V collagens used as substrates for neoplastic cell growth. Due to the complexity of a whole proteomic profile, a subset of significant protein classes was used to assess variations in protein expression levels. For this study we adop…

ProteomicsGene isoformmedicine.medical_specialtyHot TemperatureProteomeMotilityBreast NeoplasmsBiologyMatrix (biology)ProteomicsBiochemistryproteomic breast cancer cells collagenBreast cancerSettore BIO/13 - Biologia ApplicataCell Line TumorInternal medicineHeat shock protein[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyImage Processing Computer-AssistedmedicineHumansElectrophoresis Gel Two-DimensionalMolecular BiologyHeat-Shock ProteinsProteomic ProfileProteinsmedicine.diseaseCell biologyEndocrinologySpectrometry Mass Matrix-Assisted Laser Desorption-IonizationMultivariate AnalysisNeoplastic cellCollagenCell DivisionPROTEOMICS
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