Search results for "Cell Growth Processes"

showing 10 items of 24 documents

Downregulation of thioredoxin-1-dependent CD95 S-nitrosation by Sorafenib reduces liver cancer

2020

Hepatocellular carcinoma (HCC) represents 80% of the primary hepatic neoplasms. It is the sixth most frequent neoplasm, the fourth cause of cancer-related death, and 7% of registered malignancies. Sorafenib is the first line molecular targeted therapy for patients in advanced stage of HCC. The present study shows that Sorafenib exerts free radical scavenging properties associated with the downregulation of nuclear factor E2-related factor 2 (Nrf2)-regulated thioredoxin 1 (Trx1) expression in liver cancer cells. The experimental downregulation and/or overexpression strategies showed that Trx1 induced activation of nitric oxide synthase (NOS) type 3 (NOS3) and S-nitrosation (SNO) of CD95 rece…

0301 basic medicine:Anatomy::Cells::Cells Cultured::Cell Line::Cell Line Tumor [Medical Subject Headings]Factor 2 relacionado con NF-E2Regulación hacia abajomedicine.medical_treatment[SDV]Life Sciences [q-bio]Clinical Biochemistry:Chemicals and Drugs::Amino Acids Peptides and Proteins::Proteins::Thioredoxins [Medical Subject Headings]ApoptosisBiochemistry:Phenomena and Processes::Chemical Phenomena::Biochemical Phenomena::Biochemical Processes::Nitrosation [Medical Subject Headings]Targeted therapyNeoplasias hepáticas:Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Primates::Haplorhini::Catarrhini::Hominidae::Humans [Medical Subject Headings]Mice0302 clinical medicineThioredoxins:Organisms::Eukaryota::Animals [Medical Subject Headings]lcsh:QH301-705.5Cell proliferationlcsh:R5-920GSNORChemistry:Diseases::Neoplasms::Neoplasms by Site::Digestive System Neoplasms::Liver Neoplasms [Medical Subject Headings]Liver NeoplasmsSorafenibFas receptor3. Good healthHepatocellular carcinomaCD95Liver cancerlcsh:Medicine (General)NOS3Liver cancerCarcinoma hepatocelularResearch Papermedicine.drugSorafenibHepatocarcinomaProliferación celularCarcinoma HepatocellularNitrosationDown-RegulationMice Nude[SDV.CAN]Life Sciences [q-bio]/CancerAntineoplastic AgentsNrf203 medical and health sciencesDownregulation and upregulationCell Line TumormedicineAnimalsHumansS-NitrosoglutatiónTiorredoxinas:Phenomena and Processes::Cell Physiological Phenomena::Cell Physiological Processes::Cell Growth Processes::Cell Proliferation [Medical Subject Headings]:Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Rodentia::Muridae::Murinae::Mice [Medical Subject Headings]:Diseases::Neoplasms::Neoplasms by Site::Digestive System Neoplasms::Liver Neoplasms::Carcinoma Hepatocellular [Medical Subject Headings]:Phenomena and Processes::Chemical Phenomena::Biochemical Phenomena::Biochemical Processes::Down-Regulation [Medical Subject Headings]Cell growthPhenylurea CompoundsOrganic Chemistry:Chemicals and Drugs::Chemical Actions and Uses::Pharmacologic Actions::Therapeutic Uses::Antineoplastic Agents [Medical Subject Headings][SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterology:Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Rodentia::Muridae::Murinae::Mice::Mice Mutant Strains::Mice Nude [Medical Subject Headings]medicine.diseasedigestive system diseases030104 developmental biologylcsh:Biology (General)ApoptosisDownregulation:Chemicals and Drugs::Organic Chemicals::Hydrocarbons::Hydrocarbons Cyclic::Hydrocarbons Aromatic::Benzene Derivatives::Phenylurea Compounds [Medical Subject Headings][SDV.SP.PHARMA]Life Sciences [q-bio]/Pharmaceutical sciences/PharmacologyCancer researchÓxido nítrico sintasa de tipo III030217 neurology & neurosurgery
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Melatonin Targets Metabolism in Head and Neck Cancer Cells by Regulating Mitochondrial Structure and Function.

2021

This study was funded by grants from the Ministerio de Economia, Industria y Competitividad y por el Fondo de Desarrollo Regional FEDER, Spain nº SAF2013-49019, SAF2017-85903-P, and from the Consejería de Innovación, Ciencia y Empresa, Junta de Andalucía (P07- CTS- 03135, P10- CTS- 5784, and CTS- 101), Spain. J.F. and L.M. have FPU fellowships from the Ministerio de Educación Cultura y Deporte, Spain. C.R.S. was a schorlarship holder from the Plan Propio de Investigación of the University of Granada.

0301 basic medicine:Phenomena and Processes::Chemical Phenomena::Biochemical Phenomena::Biochemical Processes::Phosphorylation::Oxidative Phosphorylation [Medical Subject Headings]PhysiologyClinical BiochemistrymelatoninMitochondrionBiochemistryMelatonina:Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Primates::Haplorhini::Catarrhini::Hominidae::Humans [Medical Subject Headings]0302 clinical medicine:Anatomy::Cells::Cells Cultured::Cell Line [Medical Subject Headings]head and neck cancer cells:Phenomena and Processes::Physiological Phenomena::Pharmacological Phenomena::Drug Resistance::Drug Resistance Neoplasm [Medical Subject Headings]MitophagyMitocondriasChemistryapoptosisglycolysisOXPHOSmitochondria030220 oncology & carcinogenesishormones hormone substitutes and hormone antagonistsmedicine.drug:Phenomena and Processes::Chemical Phenomena::Biochemical Phenomena::Biochemical Processes::Carbohydrate Metabolism::Glycolysis [Medical Subject Headings]Neoplasias de cabeza y cuello:Diseases::Neoplasms::Neoplasms by Site::Head and Neck Neoplasms [Medical Subject Headings]:Chemicals and Drugs::Inorganic Chemicals::Free Radicals::Reactive Oxygen Species [Medical Subject Headings]Mitofagiafree radicalsOxidative phosphorylationArticleMelatonin03 medical and health sciencesmedicine:Phenomena and Processes::Cell Physiological Phenomena::Cell Physiological Processes::Cell Growth Processes::Cell Proliferation [Medical Subject Headings]Molecular BiologyRadicales libresCell growth:Chemicals and Drugs::Amino Acids Peptides and Proteins::Proteins::DNA-Binding Proteins::Receptors Cytoplasmic and Nuclear::Receptors Melatonin [Medical Subject Headings]:Chemicals and Drugs::Chemical Actions and Uses::Pharmacologic Actions::Therapeutic Uses::Antineoplastic Agents [Medical Subject Headings]lcsh:RM1-950:Anatomy::Cells::Cellular Structures::Subcellular Fractions::Mitochondria [Medical Subject Headings]Cell Biologymedicine.diseaseHead and neck squamous-cell carcinoma:Phenomena and Processes::Cell Physiological Phenomena::Cell Physiological Processes::Cell Death::Apoptosis [Medical Subject Headings]Glucólisis030104 developmental biologylcsh:Therapeutics. PharmacologymitophagyApoptosisCancer cellCancer research:Chemicals and Drugs::Hormones Hormone Substitutes and Hormone Antagonists::Hormones::Melatonin [Medical Subject Headings]
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9-ING-41, a small-molecule glycogen synthase kinase-3 inhibitor, is active in neuroblastoma.

2018

Advanced stage neuroblastoma is a very aggressive pediatric cancer with limited treatment options and a high mortality rate. Glycogen Synthase Kinase-3β (GSK-3β) is a potential therapeutic target in neuroblastoma. Using immunohistochemical staining, we observed positive GSK-3β expression in 67% of human neuroblastomas (34 out of 51 cases). Chemically distinct GSK-3 inhibitors (AR-A014418, TDZD8 and 9-ING-41), suppressed the growth of neuroblastoma cells whereas 9-ING-41, a clinically relevant small molecule GSK-3β inhibitor with broad spectrum pre-clinical antitumor activity, being the most potent. Inhibition of GSK-3 resulted in a decreased expression of the antiapoptotic molecule XIAP and…

0301 basic medicineCancer ResearchIndolesMice NudeCell Growth ProcessesIrinotecanArticleMaleimides03 medical and health sciencesMiceNeuroblastoma0302 clinical medicineGSK-3NeuroblastomaCell Line TumorAntineoplastic Combined Chemotherapy ProtocolsmedicineAnimalsHumansPharmacology (medical)Enzyme InhibitorsGlycogen synthasePharmacologyGlycogen Synthase Kinase 3 betabiologyChemistryDrug Synergismmedicine.diseasePediatric cancerXenograft Model Antitumor AssaysXIAP030104 developmental biologyOncologyCell cultureApoptosis030220 oncology & carcinogenesisCancer researchbiology.proteinImmunohistochemistryFemaleAnti-cancer drugs
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Different expression of thymidylate synthase in primary tumour and metastatic nodes in breast cancer patients.

2007

BACKGROUND: To date an accurate evaluation of predictive markers in breast cancer is mainly conducted at the primary site, although the main goal of the adjuvant therapy is the control of micrometastases. Adjuvant therapy drugs need a high proliferative cell rate to be effective. The proliferating activity can be evaluated by the Ki-67 marker and even by thymidylate synthase (TS), a cell cycle enzyme present in proliferating cells. In this study the TS levels in primary tumours were compared to those of their metastases. PATIENTS AND METHODS: The TS expression and Ki-67 were evaluated by means of immunohistochemistry in 80 primary breast tumours (PTs) and in their matched axillary metastati…

AdultKi-67 AntigenLymphatic MetastasisHumansBreast cancer thymidylate synthase Mib-1/Ki-67 metastatic lymph nodes.Breast NeoplasmsFemaleCell Growth ProcessesThymidylate SynthaseSettore MED/08 - Anatomia PatologicaImmunohistochemistryNeoplasm StagingAnticancer research
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Pharmacological blockade of the fatty acid amide hydrolase (FAAH) alters neural proliferation, apoptosis and gliosis in the rat hippocampus, hypothal…

2015

Endocannabinoids participate in the control of neurogenesis, neural cell death and gliosis. The pharmacological effect of the fatty acid amide hydrolase (FAAH) inhibitor URB597, which limits the endocannabinoid degradation, was investigated in the present study. Cell proliferation (phospho-H3(+) or BrdU(+) cells) of the main adult neurogenic zones as well as apoptosis (cleaved caspase-3(+)), astroglia (GFAP(+)), and microglia (Iba1(+) cells) were analyzed in the hippocampus, hypothalamus and striatum of rats intraperitoneally treated with URB597 (0.3 mg/kg/day) at one dose/4-days resting or 5 doses (1 dose/day). Repeated URB597 treatment increased the plasma levels of the N-acylethanolamine…

AstrocitosNeurobiologia del desenvolupamentAmidohidrolasasCannabinoid receptorCarbamatos:Chemicals and Drugs::Amino Acids Peptides and Proteins::Proteins::Intracellular Signaling Peptides and Proteins::Apoptosis Regulatory Proteins::Caspases [Medical Subject Headings]:Phenomena and Processes::Cell Physiological Phenomena::Cell Physiological Processes::Cell Differentiation::Neurogenesis [Medical Subject Headings]medicine.medical_treatment:Chemicals and Drugs::Carbohydrates::Monosaccharides::Hexoses::Glucose [Medical Subject Headings]Apoptosis:Phenomena and Processes::Physiological Phenomena::Body Constitution::Body Weights and Measures::Body Size::Body Weight [Medical Subject Headings]chemistry.chemical_compound:Chemicals and Drugs::Amino Acids Peptides and Proteins::Proteins::Membrane Proteins::Receptors Cell Surface::Receptors G-Protein-Coupled::Receptors Cannabinoid::Receptor Cannabinoid CB1 [Medical Subject Headings]0302 clinical medicine:Chemicals and Drugs::Organic Chemicals::Carboxylic Acids::Acids Acyclic::Carbamates [Medical Subject Headings]Fatty acid amide hydrolaseReceptor cannabinoide CB1:Organisms::Eukaryota::Animals [Medical Subject Headings]FAAHGliosishealth care economics and organizations:Chemicals and Drugs::Nucleic Acids Nucleotides and Nucleosides::Nucleosides::Deoxyribonucleosides::Deoxyuridine::Bromodeoxyuridine [Medical Subject Headings]:Chemicals and Drugs::Lipids::Glycerides::Triglycerides [Medical Subject Headings]Original Research0303 health sciencesNeurogenesisBenzamidas:Chemicals and Drugs::Polycyclic Compounds::Steroids::Cholestanes::Cholestenes::Cholesterol [Medical Subject Headings]Endocannabinoid systemEtanolaminas3. Good healthEndocannabinoides:Chemicals and Drugs::Lipids::Fatty Acids::Fatty Acids Unsaturated::Fatty Acids Monounsaturated::Oleic Acids [Medical Subject Headings]CannabinoidesMicroglíalipids (amino acids peptides and proteins)medicine.symptomColesterol:Chemicals and Drugs::Organic Chemicals::Hydrocarbons::Terpenes::Cannabinoids [Medical Subject Headings]:Chemicals and Drugs::Lipids::Fatty Acids::Palmitic Acids [Medical Subject Headings]psychological phenomena and processesProliferación celularmedicine.medical_specialtyCerebroNeurogenesiseducationBiologyBromodesoxiuridina:Anatomy::Nervous System::Neuroglia::Microglia [Medical Subject Headings]Triglicéridoslcsh:RC321-571Ácidos oléicosRatas03 medical and health sciencesCellular and Molecular NeuroscienceInternal medicineHipocampomedicineCaspasa 3:Anatomy::Nervous System::Central Nervous System::Brain::Limbic System::Hippocampus [Medical Subject Headings]:Phenomena and Processes::Cell Physiological Phenomena::Cell Physiological Processes::Cell Growth Processes::Cell Proliferation [Medical Subject Headings]lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry030304 developmental biologyPalmitoylethanolamide:Chemicals and Drugs::Chemical Actions and Uses::Pharmacologic Actions::Molecular Mechanisms of Pharmacological Action::Neurotransmitter Agents::Endocannabinoids [Medical Subject Headings]:Chemicals and Drugs::Enzymes and Coenzymes::Enzymes::Hydrolases::Amidohydrolases [Medical Subject Headings]Cannabinoids:Anatomy::Cells::Neuroglia::Astrocytes [Medical Subject Headings]Peso corporalEnergy metabolism:Anatomy::Nervous System::Central Nervous System::Brain [Medical Subject Headings]:Anatomy::Nervous System::Central Nervous System::Brain::Limbic System::Hypothalamus [Medical Subject Headings]URB597:Phenomena and Processes::Cell Physiological Phenomena::Cell Physiological Processes::Cell Death [Medical Subject Headings]:Diseases::Pathological Conditions Signs and Symptoms::Pathologic Processes::Gliosis [Medical Subject Headings]:Chemicals and Drugs::Organic Chemicals::Amines::Amino Alcohols::Ethanolamines [Medical Subject Headings]Muerte celular:Phenomena and Processes::Cell Physiological Phenomena::Cell Physiological Processes::Cell Death::Apoptosis [Medical Subject Headings]:Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Rodentia::Muridae::Murinae::Rats [Medical Subject Headings]EndocrinologyURB597chemistryGliosisnervous systemGlucosaCannabinoidEnergy Metabolism:Chemicals and Drugs::Organic Chemicals::Amides::Benzamides [Medical Subject Headings]HipotálamoÁcidos palmíticos030217 neurology & neurosurgeryNeuroscienceFrontiers in Cellular Neuroscience
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Protein kinase CK2 enables regulatory T cells to suppress excessive TH2 responses in vivo

2014

The quality of the adaptive immune response depends on the differentiation of distinct CD4(+) helper T cell subsets, and the magnitude of an immune response is controlled by CD4(+)Foxp3(+) regulatory T cells (Treg cells). However, how a tissue- and cell type-specific suppressor program of Treg cells is mechanistically orchestrated has remained largely unexplored. Through the use of Treg cell-specific gene targeting, we found that the suppression of allergic immune responses in the lungs mediated by T helper type 2 (TH2) cells was dependent on the activity of the protein kinase CK2. Genetic ablation of the β-subunit of CK2 specifically in Treg cells resulted in the proliferation of a hithert…

CD4-Positive T-LymphocytesMaleT cellImmunologyMice TransgenicReceptors Cell Surfacechemical and pharmacologic phenomenaCell Growth ProcessesT-Lymphocytes RegulatoryCell LineMiceTh2 CellsImmune systemHypersensitivitymedicineAnimalsHumansImmunology and AllergyIL-2 receptorCasein Kinase IIMice Inbred BALB CChemistryPeripheral toleranceFOXP3Cell DifferentiationForkhead Transcription FactorsDendritic CellsAcquired immune systemCell biologyMice Inbred C57BLmedicine.anatomical_structureCell cultureInterferon Regulatory FactorsImmunologyLeukocytes MononuclearIRF4Nature Immunology
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Temporal molecular and biological assessment of an erlotinib-resistant lung adenocarcinoma model reveals markers of tumor progression and treatment r…

2012

Abstract Patients with lung cancer with activating mutations in the EGF receptor (EGFR) kinase, who are treated long-term with tyrosine kinase inhibitors (TKI), often develop secondary mutations in EGFR associated with resistance. Mice engineered to develop lung adenocarcinomas driven by the human EGFR T790M resistance mutation are similarly resistant to the EGFR TKI erlotinib. By tumor volume endpoint analysis, these mouse tumors respond to BIBW 2992 (an irreversible EGFR/HER2 TKI) and rapamycin combination therapy. To correlate EGFR-driven changes in the lung with response to drug treatment, we conducted an integrative analysis of global transcriptome and metabolite profiling compared wit…

Cancer ResearchLung NeoplasmsCombination therapyAfatinibGene ExpressionAdenocarcinoma of LungCell Growth ProcessesAdenocarcinomaAfatinibArticleErlotinib HydrochlorideMiceAntineoplastic Combined Chemotherapy ProtocolsmedicineAnimalsEpidermal growth factor receptorLung cancerErlotinib HydrochlorideProtein Kinase InhibitorsSirolimusbiologymedicine.diseaserespiratory tract diseasesErbB ReceptorsOncologyTumor progressionDrug Resistance NeoplasmCancer researchbiology.proteinDisease ProgressionQuinazolinesErlotinibTyrosine kinasemedicine.drugTranscription FactorsCancer research
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Resveratrol-mediated apoptosis of hodgkin lymphoma cells involves SIRT1 inhibition and FOXO3a hyperacetylation

2012

Resveratrol (RSV), a plant-derived stilbene, induces cell death in Hodgkin lymphoma (HL)-derived L-428 cells in a dose-dependent manner (IC50 = 27 μM, trypan blue exclusion assay). At a lower range (25 μM), RSV treatment for 48 hr causes arrest in the S-phase of the cell cycle, while at a higher concentration range (50 μM), apoptosis can be detected, with activation of caspase-3. The histone/protein deacetylase SIRT1 has been described as a putative target of RSV action in other model systems, even though its role in cancer cells is still controversial. Here we show that RSV, at both concentration ranges, leads to a marked increase in p53, while a decrease of SIRT1 expression level, as well…

Cancer ResearchPathologymedicine.medical_specialtyProgrammed cell deathApoptosisCell Growth ProcessesBiologyS PhaseSirtuin 1Cell Line TumorStilbenesmedicineHumansbcl-2-Associated X ProteinB-LymphocytesDose-Response Relationship DrugCaspase 3Mantle zoneForkhead Box Protein O3Germinal centerAcetylationForkhead Transcription FactorsCell cycleGerminal CenterHodgkin DiseaseMolecular biologyOncologyResveratrolCell cultureApoptosisCancer cellLymph NodesLymphTumor Suppressor Protein p53International Journal of Cancer
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Intestinal epithelial HuR modulates distinct pathways of proliferation and apoptosis and attenuates small intestinal and colonic tumor development.

2014

Abstract HuR is a ubiquitous nucleocytoplasmic RNA-binding protein that exerts pleiotropic effects on cell growth and tumorigenesis. In this study, we explored the impact of conditional, tissue-specific genetic deletion of HuR on intestinal growth and tumorigenesis in mice. Mice lacking intestinal expression of HuR (Hur IKO mice) displayed reduced levels of cell proliferation in the small intestine and increased sensitivity to doxorubicin-induced acute intestinal injury, as evidenced by decreased villus height and a compensatory shift in proliferating cells. In the context of Apcmin/+ mice, a transgenic model of intestinal tumorigenesis, intestinal deletion of the HuR gene caused a three-fo…

Cancer ResearchPost-translational regulationRNA-binding proteinContext (language use)ApoptosisCell Growth ProcessesBiologymedicine.disease_causeArticleAU-rich RNAMiceGene expressionIntestinal NeoplasmsmedicineAnimalsmRNA stabilityIntestinal MucosaMice KnockoutCell growthMolecular biologyPhenotypeProtein-RNA interactionSmall intestineDisease Models Animalmedicine.anatomical_structureOncologyELAV ProteinsApoptosisColonic NeoplasmsCancer researchCarcinogenesis
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2-Triazenoazaindoles: Α novel class of triazenes inducing transcriptional down-regulation of EGFR and HER-2 in human pancreatic cancer cells

2012

Pancreatic cancer is a complex malignancy arising from the accumulation of genetic and epigenetic defects in the affected cells. Standard chemotherapy for patients with advanced disease shows only modest effects and is associated with considerable toxicity. Overexpression or aberrant activation of members of the epidermal growth factor receptor tyrosine kinase family, which includes EGFR and HER-2, occurs frequently and is associated with multiple drug resistance and decreased patient survival. In this study, we have investigated the therapeutic potential of AS104, a novel compound of the triazene class, with potential inhibitory effects on EGFR. We found that treatment of cells with AS104 …

Cancer ResearchProgrammed cell deathmedicine.medical_specialtyIndolesReceptor ErbB-2EGFRCellpancreatic cancer2-triazenoazaindoles pancreatic cancer cell death EGFR HER-2Down-RegulationApoptosisCell Growth ProcessesBiologyReceptor tyrosine kinasePancreatic cancerInternal medicineCell Line TumormedicineAutophagyHumansMolecular Targeted TherapyOncogeneCell growthCancerArticlesCell cyclemedicine.diseaseSettore CHIM/08 - Chimica FarmaceuticaErbB ReceptorsPancreatic Neoplasmsmedicine.anatomical_structureEndocrinologycell deathOncologyHER-2Cancer researchbiology.protein2-triazenoazaindolesTriazenesCarcinoma Pancreatic Ductal
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