Search results for "PROLIFERATION"

showing 10 items of 1193 documents

Development and biological investigations of hypoxia-sensitive prodrugs of the tyrosine kinase inhibitor crizotinib

2019

Despite the huge success of tyrosine kinase inhibitors as anticancer agents, severe side effects are a major problem. In order to overcome this drawback, the first hypoxia-activatable 2-nitroimidazole-based prodrugs of the clinically approved ALK and c-MET inhibitor crizotinib were developed. The 2-aminopyridine functionality of crizotinib (essential for target kinase binding) was considered as ideal position for prodrug derivatization. Consequently, two different prodrugs were synthesized with the nitroimidazole unit attached to crizotinib either via carbamoylation (A) or alkylation (B) of the 2-aminopyridine moiety. The successful prodrug design could be proven by docking studies and a dr…

medicine.drug_classTyrosine kinase inhibitorAntineoplastic Agents01 natural sciencesBiochemistryArticleTyrosine-kinase inhibitorStructure-Activity Relationshipchemistry.chemical_compoundDrug DevelopmentCrizotinibIn vivoDrug DiscoverymedicineHumansAnaplastic Lymphoma KinaseProdrugsHypoxiaProdrugProtein Kinase InhibitorsMolecular BiologyCells CulturedCell ProliferationNitroimidazoleDose-Response Relationship DrugMolecular StructureCrizotinib010405 organic chemistryChemistryNitroimidazoleOrganic ChemistryProto-Oncogene Proteins c-metProdrugCell Hypoxia0104 chemical sciences010404 medicinal & biomolecular chemistrySettore CHIM/03 - Chimica Generale E InorganicaDocking (molecular)Cancer researchDrug Screening Assays AntitumorKinase bindingTyrosine kinasemedicine.drugBioorganic Chemistry
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Topical application of the adenosine A2Areceptor agonist CGS-21680 prevents phorbol-induced epidermal hyperplasia and inflammation in mice

2014

The nucleoside adenosine is a known regulator of immunity and inflammation that mediates, at least in part, the anti-inflammatory effect of methotrexate, an immunosuppressive agent widely used to treat autoimmune inflammatory diseases. Adenosine A2A receptors play a key role in the inhibition of the inflammatory process besides promoting wound healing. Therefore, we aimed to determine the topical effect of a selective agonist, CGS-21680, on a murine model of skin hyperplasia with a marked inflammatory component. Pretreatment with either CGS-21680 (5 μg per site) or the reference agent dexamethasone (200 μg/site) prevented the epidermal hyperplasia and inflammatory response induced by topica…

medicine.medical_specialtyAdenosineAdenosine A2 Receptor AgonistsAdministration Topicalmedicine.medical_treatmentAnti-Inflammatory AgentsAdenosine A2A receptorInflammationDermatologyPharmacologyBiologySkin DiseasesBiochemistryDexamethasoneMicechemistry.chemical_compoundInternal medicinePhenethylaminesmedicineAnimalsMolecular BiologyDexamethasoneCell ProliferationPeroxidaseCGS-21680InflammationHyperplasiaAdenosineAdenosine receptorDisease Models AnimalEndocrinologyCytokinechemistryCytokinesTetradecanoylphorbol AcetateFemaleCollagenEpidermismedicine.symptomWound healingmedicine.drugExperimental Dermatology
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Inhibition of Delta-like 4 mediated signaling induces abortion in mice due to deregulation of decidual angiogenesis.

2013

Objective: To explore whether the Dll4/Notch1 pathway plays a key role in regulating the vascular endothelial growth factor (VEGF)/VEGF receptor 2 (VEGFR2) driven decidual angiogenesis and related pregnancy through induction of a tip/stalk phenotype. Methods: Progesterone-replaced ovariectomized pregnant mice received a single injection of YW152F (Dll4 blocking antibody, BAb) or placebo at embryonic day (E) 4.5. Animals were sacrificed at different time points; blood and uterus were collected for further analysis. Number of embryos and implantation site, uteri weight, and serum progesterone levels were assessed. Alterations in the tip/stalk phenotype were determined by quantitative immunofl…

medicine.medical_specialtyAngiogenesisNotch pathwayNotch signaling pathwayUterusEmbryonic DevelopmentNeovascularization PhysiologicApoptosisGestational AgeDll4BiologyPregnancy disruptionAndrologychemistry.chemical_compoundMicePregnancyInternal medicinemedicineDeciduaAnimalsAntibodies BlockingAdaptor Proteins Signal TransducingCell ProliferationCell growthDeciduaCalcium-Binding ProteinsIntracellular Signaling Peptides and ProteinsObstetrics and GynecologyMembrane ProteinsEmbryoVEGFVascular Endothelial Growth Factor Receptor-2Vascular endothelial growth factorDisease Models Animalmedicine.anatomical_structureEndocrinologyReproductive MedicinechemistryApoptosiscardiovascular systemEmbryo LossFemaleAngiogenesisDevelopmental BiologySignal TransductionPlacenta
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Analysis of molecular mechanisms and anti-tumoural effects of zoledronic acid in breast cancer cells

2012

Zoledronic acid (ZOL) is the most potent nitrogen-containing bisphosphonate (N-BPs) that strongly binds to bone mineral and acts as a powerful inhibitor of bone resorption, already clinically available for the treatment of patients with osteolytic metastases. Recent data also suggest that ZOL, used in breast cancer, may provide more than just supportive care modifying the course of the disease, though the possible molecular mechanism of action is still unclear. As breast cancer is one of the primary tumours with high propensity to metastasize to the bone, we investigated, for the first time, differential gene expression profile on Michigan Cancer Foundation-7 (MCF-7) breast cancer cells tre…

medicine.medical_specialtyAngiogenesismedicine.medical_treatmentBlotting WesternAngiogenesis InhibitorsAntineoplastic AgentsBreast NeoplasmsBiologyReal-Time Polymerase Chain ReactionZoledronic AcidZOL FN1 TGF-b1 THBS-1 invasion breast cancerBone resorptionThrombospondin 1Transforming Growth Factor beta1breast cancerBreast cancerTGF-β1Internal medicineThrombospondin 1medicineHumansBone ResorptionCell ProliferationMatrigelDiphosphonatesFN1Gene Expression ProfilingImidazolesCancerOriginal ArticlesCell BiologyZOLBisphosphonateMicroarray Analysisinvasionmedicine.diseaseFibronectinsUp-RegulationGene Expression Regulation NeoplasticEndocrinologyZoledronic acidTHBS-1MCF-7 CellsCancer researchMolecular MedicineFemalemedicine.drug
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Differential miRNA expression defines migration and reduced apoptosis in follicular thyroid carcinomas.

2013

The objective of the study was to identify microRNAs (miRs) characteristic for follicular thyroid carcinoma (FTC) and to define their role in tumorigenesis. A miR-microarray study was conducted to identify miRs differentially expressed between FTCs and their surrounding tissues. Selection was further reinforced by a literature review. Four miRs were selected and confirmed by RT-qPCR: miR-146b, -183, -221 were up-regulated, whereas miR-199b down-regulated in FTCs. The influence of these miRs on cell proliferation, cell cycle, apoptosis and migration was studied in HTori and FTC-133 cells. Functional characterization suggests an impact of miR-183 and miR-146b in FTC development. Overexpressio…

medicine.medical_specialtyApoptosisBiologymedicine.disease_causeBiochemistryThyroid carcinomaEndocrinologyCell MovementInternal medicineCell Line TumorFollicular phasemicroRNAAdenocarcinoma FollicularmedicineHumansThyroid NeoplasmsFollicular thyroid cancerMolecular BiologyCell ProliferationCell growthCell cyclemedicine.diseaseGene Expression Regulation NeoplasticMicroRNAsEndocrinologyApoptosisCancer researchCarcinogenesisMolecular and cellular endocrinology
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Amphiregulin activates human hepatic stellate cells and is upregulated in non alcoholic steatohepatitis

2015

AbstractAmphiregulin (AR) involvement in liver fibrogenesis and hepatic stellate cells (HSC) regulation is under study. Non-alcoholic fatty liver disease (NAFLD) and its more severe form non-alcoholic steatohepatitis (NASH) may progress to cirrhosis and hepatocellular cancer (HCC). Our aim was to investigate ex vivo the effect of AR on human primary HSC (hHSC) and verify in vivo the relevance of AR in NAFLD fibrogenesis. hHSC isolated from healthy liver segments were analyzed for expression of AR and its activator, TNF-α converting enzyme (TACE). AR induction of hHSC proliferation and matrix production was estimated in the presence of antagonists. AR involvement in fibrogenesis was also ass…

medicine.medical_specialtyBiopsyGene ExpressionADAM17 ProteinBiologyAmphiregulinSeverity of Illness Indexp38 Mitogen-Activated Protein Kinasesdigestive systemArticleMicePhosphatidylinositol 3-Kinases03 medical and health sciences0302 clinical medicineDownregulation and upregulationAmphiregulinGrowth factor receptorNon-alcoholic Fatty Liver DiseaseInternal medicineHepatic Stellate CellsmedicineAnimalsHumansProtein Kinase CPI3K/AKT/mTOR pathwayCell Proliferation030304 developmental biology0303 health sciencesMultidisciplinaryFatty livernutritional and metabolic diseasesmedicine.diseaseFibrosisActinsdigestive system diseases3. Good healthEnzyme ActivationErbB ReceptorsADAM ProteinsDisease Models AnimalEndocrinologyHepatic stellate cellCancer research030211 gastroenterology & hepatologyTumor necrosis factor alphaCollagenSteatohepatitisSignal TransductionScientific Reports
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Histamine and spontaneously released mast cell granules affect the cell growth of human hepatocellular carcinoma cells

2007

The role of mast cells in tumor growth is still controversial. In this study we analyzed the effects of both histamine and pre-formed mediators spontaneously released by mast cells on the growth of two human hepatocellular carcinoma cell lines, HA22T/VGH and HuH-6, with different characteristics of differentiation, biological behavior and genetic defects. We showed that total mast cell releasate, exocytosed granules (granule remnants) and histamine reduced cell viability and proliferation in HuH-6 cells. In contrast, in HA22T/VGH cells granule remnants and histamine induced a weak but significant increase in cell growth. We showed that both cell lines expressed histamine receptors H(1) and …

medicine.medical_specialtyCarcinoma HepatocellularCell SurvivalSurvivinClinical BiochemistryHistamine AntagonistsApoptosisHistamine H1 receptorBiologyRanitidineBiochemistryExocytosisInhibitor of Apoptosis ProteinsHistamine receptorchemistry.chemical_compoundInternal medicineCell Line TumormedicineAnimalsHumansHistamine H4 receptorMast CellsEnterochromaffin-like cellRats WistarMolecular BiologyCells Culturedbeta CateninCell ProliferationCell growthCaspase 3Liver NeoplasmsMast cellMolecular biologyNeoplasm ProteinsRatsEnzyme ActivationEndocrinologymedicine.anatomical_structurechemistryCell cultureCyclooxygenase 2Molecular MedicineReceptors HistamineFemaleTerfenadinePoly(ADP-ribose) PolymerasesMicrotubule-Associated ProteinsHistamineHistamine
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Medical significance of peroxisome proliferator-activated receptors.

1999

Peroxisome proliferator-activated receptors (PPAR) were discovered in 1990, ending 25 years of uncertainty about the molecular mechanisms of peroxisome proliferation. Subsequently, PPARs have improved our understanding of adipocyte differentiation. But there is more to PPARs than solving a puzzle about an organelle (the peroxisome) long considered an oddity, and their medical significance goes beyond obesity too. Enhanced PPAR type alpha expression protects against cardiovascular disorders though the role of enhanced PPARgamma expression seems less favourable. PPAR mechanisms, mainly via induction of more differentiated cell phenotypes, protect against some cancers. The differentiation of m…

medicine.medical_specialtyCellular differentiationPeroxisome ProliferationPeroxisome proliferator-activated receptorReceptors Cytoplasmic and NuclearBiologyMicrobodiesInternal medicineNeoplasmsmedicineAdipocytesAnimalsHumansReceptorRegulation of gene expressionchemistry.chemical_classificationResearchFatty AcidsCell DifferentiationGeneral MedicinePeroxisomeEndocrinologychemistryNuclear receptorGene Expression RegulationCardiovascular DiseasesCancer researchPeroxisome proliferator-activated receptor alphaOxidation-ReductionTranscription FactorsLancet (London, England)
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Developmental and tumoral vascularization is regulated by G protein-coupled receptor kinase 2

2012

Tumor vessel dysfunction is a pivotal event in cancer progression. Using an in vivo neovascularization model, we identified G protein–coupled receptor kinase 2 (GRK2) as a key angiogenesis regulator. An impaired angiogenic response involving immature vessels was observed in mice hemizygous for Grk2 or in animals with endothelium-specific Grk2 silencing. ECs isolated from these animals displayed intrinsic alterations in migration, TGF-β signaling, and formation of tubular networks. Remarkably, an altered pattern of vessel growth and maturation was detected in postnatal retinas from endothelium-specific Grk2 knockout animals. Mouse embryos with systemic or endothelium-selective Grk2 ablation …

medicine.medical_specialtyG-Protein-Coupled Receptor Kinase 2Angiogenic SwitchAngiogenesisMedicinaActivin Receptors Type IIMelanoma ExperimentalReceptor Transforming Growth Factor-beta Type INeovascularization PhysiologicProtein Serine-Threonine KinasesBiologyMural cellGrk2Transforming Growth Factor beta1NeovascularizationMiceDownregulation and upregulationCell MovementPregnancyInternal medicinemedicineAnimalsHumansCell ProliferationHemizygoteMice KnockoutG protein-coupled receptor kinaseTumorNeovascularization PathologicEndothelial CellsRetinal VesselsG proteinGeneral MedicineCell biologyEndocrinologymedicine.anatomical_structurecardiovascular systemFemalePericyteSignal transductionmedicine.symptomActivin Receptors Type IReceptors Transforming Growth Factor betaSignal TransductionResearch Article
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Diacylglycerol kinase α mediatses 17-β-estradiol-induced proliferation, motility, and anchorage-independent growth of Hec-1A endometrial cancer cell …

2011

Increased levels of endogenous and/or exogenous estrogens are one of the well known risk factors of endometrial cancer. Diacylglycerol kinases (DGKs) are a family of enzymes which phosphorylate diacylglycerol (DAG) to produce phosphatidic acid (PA), thus turning off and on DAG-mediated and PA-mediated signaling pathways, respectively. DGK α activity is stimulated by growth factors and oncogenes and is required for chemotactic, proliferative, and angiogenic signaling in vitro. Herein, using either specific siRNAs or the pharmacological inhibitor R59949, we demonstrate that DGK α activity is required for 17-β-estradiol (E2)-induced proliferation, motility, and anchorage-independent growth of …

medicine.medical_specialtyGPR30medicine.drug_classCell SurvivalDiacylglycerol kinaseMotilityEstrogen receptorEnzyme AssayEndometrial carcinomaBiologyQuinazolinoneReceptors G-Protein-CoupledPiperidinePiperidinesCell MovementInternal medicineCell Line TumormedicineCell AdhesionHumansEndometrial NeoplasmEnzyme AssaysQuinazolinonesDiacylglycerol kinaseCell ProliferationEstradiolCell growthKinaseCell BiologyDiacylglycerol kinase; Endometrial carcinoma; Estrogen; GPR30; Cell BiologyEstrogenEndometrial NeoplasmsCell biologyEnzyme ActivationLipoprotein LipaseEndocrinologyReceptors EstrogenEstrogenGene Knockdown TechniquesGene Knockdown TechniqueFemaleRNA InterferenceSignal transductionGPERHuman
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