Search results for "PROLIFERATION"

showing 10 items of 1193 documents

Cancer-associated fibroblasts do not respond to combined irradiation and kinase inhibitor treatment

2012

The emergence of radioresistance is a significant issue in the treatment of squamous cell carcinoma. We recently demonstrated that post-radiogenic extracellular signal-regulated kinase (ERK) signaling might decrease radiosensitivity in this cancer type. To further elucidate how tumor-organizing cell types respond to irradiation and ERK pathway inhibition, we analyzed one oral squamous cell carcinoma and one lung cancer cell line (HNSCCUM-02T, A549), fibroblasts (NIH3T3), primary normal and cancer-associated fibroblasts (CAFs) in vitro. Irradiated cells treated with mitogen-activated protein kinase (MAPK) inhibitor U0126 were screened for pERK levels. Post-radiogenic cellular responses were …

MAPK/ERK pathwayCancer ResearchLung NeoplasmsCell SurvivalMAP Kinase Signaling SystemBiologyRadiation DosageRadiation ToleranceMiceCarcinoma Non-Small-Cell LungCell Line TumorRadioresistanceNitrilesButadienesmedicineAnimalsHumansExtracellular Signal-Regulated MAP KinasesProtein kinase AFibroblastProtein Kinase InhibitorsTumor Stem Cell AssayCell ProliferationOncogeneKinaseGeneral MedicineFibroblastsCell cycleMolecular biologymedicine.anatomical_structureOncologyCarcinoma Squamous CellNIH 3T3 CellsCancer researchCancer-Associated FibroblastsMouth NeoplasmsOncology Reports
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Effects of two organotin(IV)(sulfonato phenyl)porphynates on the MAPKs and on the growth of A375 human melanoma cells

2009

Previously we showed apoptotic induction in A375 human melanoma cells using two complexes of the meso-tetra(4-sulfonatophenyl)porphinate (TPPS), (Bu 2 Sn) 2 TPPS and (Bu 3 Sn) 4 TPPS. To understand how these compounds activate apoptosis in melanoma cells we studied MAPKs and the (Bu 2 Sn) 2 TPPS and (Bu 3 Sn) 4 TPPS cellular uptake. Western blotting experiments showed activated protein kinases ERK 1/2, JNK and p38 in 10 μM (Bu 2 Sn) 2 TPPS- and 1 μM (Bu 3 Sn) 4 TPPS-treated melanoma cells, which suggests that the three MAP kinases are involved in the apoptotic death of A375-treated cells. By taking advantage of the porphyrin fluorescence, we found a fast concentration of (Bu 2 Sn) 2 TPPS an…

MAPK/ERK pathwayCancer ResearchPorphyrinsp38 mitogen-activated protein kinasesBlotting WesternAntineoplastic AgentsApoptosischemistry.chemical_compoundCell Line TumorOrganotin CompoundsHumansMelanomaCell ProliferationbiologyKinaseCell growthGeneral MedicineA375 melamoma cells meso-tetra(4-sulfonato phenyl)porphinate MAPKs FAK cell growthMolecular biologyPorphyrinIn vitroMicroscopy Fluorescence MultiphotonOncologyBiochemistrychemistryApoptosisSettore CHIM/03 - Chimica Generale E InorganicaMitogen-activated protein kinasebiology.proteinMitogen-Activated Protein Kinases
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Emerging MEK inhibitors

2010

IMPORTANCE OF THE FIELD: The Ras/Raf/MEK/ERK pathway is often activated by genetic alterations in upstream signaling molecules. Integral components of this pathway such as Ras and B-Raf are also activated by mutation. The Ras/Raf/MEK/ERK pathway has profound effects on proliferative, apoptotic and differentiation pathways. This pathway can often be effectively silenced by MEK inhibitors. AREAS COVERED BY THIS REVIEW: This review will discuss targeting of MEK which could lead to novel methods to control abnormal proliferation which arises in cancer and other proliferative diseases. This review will cover the scientific literature from 1980 to present and is a follow on from a review which fo…

MAPK/ERK pathwayCell signalingAntineoplastic Agentsmedicine.disease_causemekerkEnzyme activatorNeoplasmsAntineoplastic Combined Chemotherapy ProtocolsmedicineAnimalsHumansPharmacology (medical)Protein phosphorylationProtein Kinase InhibitorsMEK inhibitorsCell ProliferationCancerPharmacologyapoptosis; cancer; erk; kinases; mek; mek inhibitors; proliferative disorders; protein phosphorylation; signal transductionproliferative disordersMutationKinasebusiness.industryapoptosisApoptosiCancerDrugs InvestigationalMAP Kinase Kinase Kinasesmedicine.diseaseprotein phosphorylationCell biologyEnzyme ActivationTreatment OutcomekinasesChemotherapy AdjuvantRadiotherapy AdjuvantSignal transductionbusinesssignal transductionExpert Opinion on Emerging Drugs
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Regulation of ERK1/2 activity upon contact inhibition in fibroblasts.

2011

Contact inhibition is a crucial mechanism regulating proliferation in vitro and in vivo. Despite its generally accepted importance for maintaining tissue homeostasis knowledge about the underlying molecular mechanisms of contact inhibition is still scarce. Since the MAPK ERK1/2 plays a pivotal role in the control of proliferation, we investigated regulation of ERK1/2 phosphorylation which is downregulated in confluent NIH3T3 cultures. We found a decrease in upstream signaling including phosphorylation of the growth factor receptor adaptor protein ShcA and the MAPK kinase MEK1/2 in confluent compared to exponentially growing cultures whereas involvement of ERK1/2 phosphatases in ERK1/2 inact…

MAPK/ERK pathwayCell signalingBiophysicsDown-RegulationCell CommunicationBiochemistryReceptor Platelet-Derived Growth Factor betaMiceGrowth factor receptorAnimalsReceptors Platelet-Derived Growth FactorPhosphorylationMolecular BiologyTissue homeostasisCell ProliferationMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3biologySignal transducing adaptor proteinContact inhibitionCell BiologyFibroblastsMolecular biologyCell biologyErbB Receptorsbiology.proteinNIH 3T3 CellsPhosphorylationPlatelet-derived growth factor receptorBiochemical and biophysical research communications
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Docosahexaenoic acid inhibits cancer cell growth via p27Kip1, CDK2, ERK1/ERK2, and retinoblastoma phosphorylation

2006

Docosahexaenoic acid (DHA), a PUFA of the n-3 family, inhibited the growth of FM3A mouse mammary cancer cells by arresting their progression from the late-G(1) to the S phase of the cell cycle. DHA upregulated p27(Kip1) levels by inhibiting phosphorylation of mitogen-activated protein (MAP) kinases, i.e., ERK1/ERK2. Indeed, inhibition of ERK1/ERK2 phosphorylation by DHA, U0126 [chemical MAPK extracellularly signal-regulated kinase kinase (MEK) inhibitor], and MEK(SA) (cells expressing dominant negative constructs of MEK) resulted in the accumulation of p27(Kip1). MAP kinase (MAPK) inhibition by DHA did not increase p27(Kip1) mRNA levels. Rather, this fatty acid stabilized p27(Kip1) contents…

MAPK/ERK pathwayDocosahexaenoic AcidsMammary Neoplasms AnimalQD415-436fatty acidsenvironment and public healthBiochemistryMiceEndocrinologyCyclin-dependent kinaseCyclin EAnimalsRNA MessengerPhosphorylationCells CulturedCell ProliferationMAPK14biologyKinaseCyclin-dependent kinase 4Cyclin-Dependent Kinase 2Cyclin-dependent kinase 2Retinoblastomafood and beveragesCell BiologyUp-RegulationCell biologyenzymes and coenzymes (carbohydrates)cyclin-dependent kinaseCyclin-dependent kinase complexbiology.proteinPhosphorylationcell cyclelipids (amino acids peptides and proteins)Mitogen-Activated Protein KinasesCyclin-Dependent Kinase Inhibitor p27Journal of Lipid Research
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Acidosis induces multi-drug resistance in rat prostate cancer cells (AT1) in vitro and in vivo by increasing the activity of the p-glycoprotein via a…

2008

Because solid growing tumors often show hypoxia and pronounced extracellular acidosis, the aim of this study was to analyze the impact of an acidotic environment on the activity of the p-glycoprotein (pGP) and on the cellular content and cytotoxicity of the chemotherapeutic drug daunorubicin in the AT1 R-3327 Dunning prostate carcinoma cell line cultured in vitro and in vivo. In vitro, extracellular acidosis (pH 6.6) activated p38 and ERK1/2 and thereby induced daunorubicin resistance via a pronounced activation of pGP. De-novo protein synthesis was not necessary and analysis of transport kinetics indicated a fast and persistent pGP activation at pH 6.6 (when compared with 7.4). Intracellul…

MAPK/ERK pathwayMaleCancer Researchmedicine.medical_specialtyDaunorubicinPharmacologyp38 Mitogen-Activated Protein KinasesIn vivoInternal medicinepolycyclic compoundsmedicineExtracellularAnimalsATP Binding Cassette Transporter Subfamily B Member 1Extracellular Signal-Regulated MAP KinasesProtein Kinase CP-glycoproteinAcidosisCell ProliferationbiologyCaspase 3DaunorubicinProstatic NeoplasmsBiological activityHydrogen-Ion ConcentrationIn vitroDrug Resistance MultipleRatscarbohydrates (lipids)Enzyme ActivationEndocrinologyOncologyDrug Resistance Neoplasmbiology.proteinmedicine.symptomAcidosisNeoplasm Transplantationmedicine.drugInternational journal of cancer
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Erythropoietin activates cell survival pathways in breast cancer stem-like cells to protect them from chemotherapy

2013

Abstract Recombinant erythropoietin (EPO) analogs [erythropoiesis-stimulating agents (ESA)] are clinically used to treat anemia in patients with cancer receiving chemotherapy. After clinical trials reporting increased adverse events and/or reduced survival in ESA-treated patients, concerns have been raised about the potential role of ESAs in promoting tumor progression, possibly through tumor cell stimulation. However, evidence is lacking on the ability of EPO to directly affect cancer stem–like cells, which are thought to be responsible for tumor progression and relapse. We found that breast cancer stem–like cells (BCSC) isolated from patient tumors express the EPO receptor and respond to …

MAPK/ERK pathwayOncologyCancer Researchmedicine.medical_treatmentFluorescent Antibody TechniqueApoptosisMice SCIDImmunoenzyme TechniquesMiceCell MovementMice Inbred NODhemic and lymphatic diseasesTumor Cells CulturedCulturedBlottingAnemiaFlow CytometryTumor CellsTRIALSOncologyDisease ProgressionNeoplastic Stem CellsFemaleWesternSignal Transductionmedicine.drugSTIMULATING AGENTSEXPRESSIONmedicine.medical_specialtyBlotting WesternAntineoplastic AgentsBreast NeoplasmsSCIDRECOMBINANT-HUMAN-ERYTHROPOIETIN STIMULATING AGENTS EXPRESSION MORTALITY TRIALS ANEMIA ALPHA ALDH1Breast cancerIn vivoInternal medicinemedicineAnimalsHumansBreast cancer Cancer stem cellsALDH1ErythropoietinProtein kinase BCell ProliferationSettore MED/04 - Patologia GeneraleChemotherapybusiness.industryMORTALITYCancerRECOMBINANT-HUMAN-ERYTHROPOIETINmedicine.diseaseALPHAErythropoietinTumor progressionInbred NODAnemia; Animals; Antineoplastic Agents; Apoptosis; Blotting Western; Breast Neoplasms; Cell Movement; Cell Proliferation; Disease Progression; Erythropoietin; Female; Flow Cytometry; Fluorescent Antibody Technique; Humans; Immunoenzyme Techniques; Mice; Mice Inbred NOD; Mice SCID; Neoplastic Stem Cells; Signal Transduction; Tumor Cells Cultured; Cancer Research; Oncologybusiness
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Ability of nanocrystalline hydroxyapatite paste to promote human periodontal ligament cell proliferation.

2008

Recent studies indicate that nanocrystalline hydroxyapatite (nano-HA) paste represents a promising class of bone graft substitute. However, the underlying molecular mechanisms of nano-HA function have not yet been determined. This study was conducted to investigate the proliferation of human periodontal ligament (PDL) cells cultured in the presence of nano-HA paste and to characterize associated changes in intracellular signaling pathways. Cultured PDL cells were stimulated with nano-HA paste and enamel matrix derivative (EMD) in a soluble form. Proliferation of PDL cells was determined by incorporation of bromodeoxyuridine (BrdU) in the DNA of proliferating cells. In order to understand th…

MAPK/ERK pathwayPeriodontal LigamentBlotting Westernchemistry.chemical_compoundDental Enamel ProteinsPeriodontal fiberHumansRegenerationEpidermal growth factor receptorPhosphorylationGeneral DentistryProtein kinase BCells CulturedCell ProliferationMitogen-Activated Protein Kinase 1biologyChemistryCell growthKinaseAnatomyFibroblastsCell biologyErbB ReceptorsDurapatiteBone Substitutesbiology.proteinPhosphorylationNanoparticlesProto-Oncogene Proteins c-aktBromodeoxyuridineJournal of oral science
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Differences in cell proliferation in rodent and human hepatic derived cell lines exposed to ciprofibrate.

2005

International audience; Humans appear to be refractory to some effects of peroxisome proliferators including alterations in cell proliferation, whereas rodents are susceptible. In this study, differences between the human and rat response to peroxisome proliferators were evaluated using rat and human tumour liver cell lines. Rat 7777 cells were more responsive than human HepG2 cells to ciprofibrate as they exhibited a higher decrease in cell number than HepG2, and underwent apoptosis. Results from these studies reveal a surprising response in tumour cell lines as the typical in vivo response of increased cell proliferation and reduced apoptosis was not observed in rat tumour cell lines at c…

MESH : Cell LineCancer ResearchRodentApoptosisMESH : Dose-Response Relationship DrugCell LineClofibric AcidIn vivobiology.animalmedicineMESH : Cell ProliferationAnimals[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyCell ProliferationHypolipidemic AgentsDose-Response Relationship DrugbiologyCell growthMESH : RatsFibric AcidsMESH : LiverMESH : Clofibric AcidRatsCell biologyLiverOncologyApoptosisCell cultureHepg2 cellsCancer researchPeroxisome proliferator-activated receptor alphaCiprofibrateMESH : AnimalsMESH : Apoptosismedicine.drugMESH : Antilipemic Agents
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CD4+CD25+ regulatory T cells inhibit natural killer cell functions in a transforming growth factor-beta-dependent manner.

2007

Tumor growth promotes the expansion of CD4+CD25+ regulatory T (T reg) cells that counteract T cell–mediated immune responses. An inverse correlation between natural killer (NK) cell activation and T reg cell expansion in tumor-bearing patients, shown here, prompted us to address the role of T reg cells in controlling innate antitumor immunity. Our experiments indicate that human T reg cells expressed membrane-bound transforming growth factor (TGF)–β, which directly inhibited NK cell effector functions and down-regulated NKG2D receptors on the NK cell surface. Adoptive transfer of wild-type T reg cells but not TGF-β−/− T reg cells into nude mice suppressed NK cell–mediated cytotoxicity, redu…

MESH : CytokinesMESH: Flow CytometryMESH : Immunity NaturalMESH: T-LyLymphocyte ActivationT-Lymphocytes RegulatoryMiceInterleukin 210302 clinical medicineT-Lymphocyte SubsetsTransforming Growth Factor betaNeoplasmsMESH : Receptors ImmunologicMESH : Cell ProliferationImmunology and Allergy[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyMESH: AnimalsMESH: NeoplasmsIL-2 receptorReceptors Immunologic0303 health sciencesMESH: Cytokineshemic and immune systemsFlow CytometryNatural killer T cell3. Good healthCell biologyKiller Cells Naturalmedicine.anatomical_structureNK Cell Lectin-Like Receptor Subfamily KInterleukin 12CytokinesReceptors Natural Killer Cell[SDV.IMM]Life Sciences [q-bio]/ImmunologyFranceMESH : Killer Cells NaturalMESH : Cytotoxicity Tests ImmunologicMESH: Killer Cells NaturalMESH: Cell Line TumorMESH : Flow CytometryImmunologychemical and pharmacologic phenomenaMESH: Cytotoxicity Tests ImmunologicMESH : Mice Inbred C57BLBiologyArticleNatural killer cell03 medical and health sciencesMESH: Mice Inbred C57BLCell Line TumorMESH: Cell ProliferationMESH : MicemedicineAnimalsHumansAntigen-presenting cellMESH: Lymphocyte ActivationMESH : FranceMESH: MiceMESH: Receptors ImmunologicMESH : Lymphocyte ActivationCell Proliferation030304 developmental biologyMESH: Immunity NaturalLymphokine-activated killer cellMESH: HumansMESH : Cell Line TumorMESH : HumansCytotoxicity Tests ImmunologicNKG2DMESH : T-LyMESH : NeoplasmsImmunity InnateMice Inbred C57BLMESH: FranceMESH : Animals030215 immunology
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