Search results for " Neoplastic"

showing 10 items of 662 documents

Socs3 induction by PPARγ restrains cancer-promoting inflammation

2013

The presence of proinflammatory cytokines in the tumor microenvironment can support further growth of established cancers. Docosahexaenoic acid (DHA), a peroxisome proliferator-activated receptor-gamma (PPARγ) ligand, has been shown to suppress inflammation and limit tumor progression in vivo. Are the anticancer properties of DHA relying on its ability to prevent inflammation? If so, what are the molecular links between the anti-inflammatory properties of DHA and its anticancer effects? DHA is an n-3 polyinsaturated fatty acid mainly found in fish oil that was shown to contribute to inflammation resolution by preventing the release of proinflammatory mediators in vivo.1 DHA has also been as…

STAT3 Transcription FactorDocosahexaenoic AcidsCellular differentiationPeroxisome proliferator-activated receptorInflammationSuppressor of Cytokine Signaling ProteinsBiologyEditorials: Cell Cycle FeaturesProinflammatory cytokineMicemedicineAnimalsHumansPhosphorylationPromoter Regions GeneticMolecular BiologyCells Culturedchemistry.chemical_classificationInflammationTumor microenvironmentInterleukin-17TroglitazoneCell DifferentiationCell BiologyPPAR gammaCell Transformation NeoplasticchemistryGene Expression RegulationSuppressor of Cytokine Signaling 3 ProteinImmunologyCancer cellCancer researchTh17 CellsInterleukin 17medicine.symptomDevelopmental Biologymedicine.drugProtein BindingSignal TransductionCell Cycle
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Tumor-Derived Small Extracellular Vesicles Induce Pro-Inflammatory Cytokine Expression and PD-L1 Regulation in M0 Macrophages via IL-6/STAT3 and TLR4…

2021

Tumor-associated macrophages play a key role in promoting tumor progression by exerting an immunosuppressive phenotype associated with the expression of programmed cell death ligand 1 (PD-L1). It is well known that tumor-derived small extracellular vesicles (SEVs) affect the tumor microenvironment, influencing TAM behavior. The present study aimed to examine the effect of SEVs derived from colon cancer and multiple myeloma cells on macrophage functions. Non-polarized macrophages (M0) differentiated from THP-1 cells were co-cultured with SEVs derived from a colorectal cancer (CRC) cell line, SW480, and a multiple myeloma (MM) cell line, MM1.S. The expression of PD-L1, interleukin-6 (IL-6), a…

STAT3 Transcription FactorPD-L1QH301-705.5colorectal cancersmall extracellular vesiclesB7-H1 AntigenArticleCatalysisStat3 Signaling PathwayProinflammatory cytokineM0 macrophageInorganic ChemistryExtracellular VesiclesSettore BIO/13 - Biologia ApplicataCell Line TumorPD-L1Tumor-Associated Macrophagessmall extracellular vesicleHumansMacrophageTLR4Biology (General)Physical and Theoretical ChemistryM0 macrophagesQD1-999Molecular BiologySpectroscopyInflammationTumor microenvironmentbiologyInterleukin-6ChemistryOrganic ChemistryGeneral MedicineComputer Science ApplicationsGene Expression Regulation NeoplasticToll-Like Receptor 4multiple myelomaChemistryCell cultureTumor progressionColonic Neoplasmsbiology.proteinCancer researchTLR4Signal TransductionInternational Journal of Molecular Sciences
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Inhibition of VEGF expression through blockade of Hif1a and STAT3 signalling mediates the anti-angiogenic effect of melatonin in HepG2 liver cancer c…

2013

Background: Hepatocellular carcinoma (HCC) growth relies on angiogenesis via vascular endothelial growth factor (VEGF) release. Hypoxia within tumour environment leads to intracellular stabilisation of hypoxia inducible factor 1 alpha (Hif1α) and signal transducer and activator of transcription (STAT3). Melatonin induces apoptosis in HCC, and shows anti-angiogenic features in several tumours. In this study, we used human HepG2 liver cancer cells as an in vitro model to investigate the anti-angiogenic effects of melatonin. Methods: HepG2 cells were treated with melatonin under normoxic or CoCl2-induced hypoxia. Gene expression was analysed by RT–qPCR and western blot. Melatonin-induced anti-…

STAT3 Transcription FactorTranscriptional ActivationVascular Endothelial Growth Factor ACancer ResearchCarcinoma HepatocellularTranscription GeneticAngiogenesisAngiogenesis InhibitorsApoptosismelatoninP300-CBP Transcription FactorsHif1αBiologyMelatoninSTAT3chemistry.chemical_compoundHypoxia-Inducible Factor 1-AlphamedicineHuman Umbilical Vein Endothelial CellsHumansp300-CBP Transcription FactorsSTAT3Promoter Regions GeneticTube formationNeovascularization PathologicLiver NeoplasmsCobaltHep G2 Cellshepatocellular carcinomaHypoxia-Inducible Factor 1 alpha SubunitVEGFCell Hypoxiadigestive system diseasesCyclic S-OxidesVascular endothelial growth factorGene Expression Regulation NeoplasticVascular endothelial growth factor AOncologychemistryCancer researchbiology.proteinTranslational Therapeuticsmedicine.drugSignal Transduction
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miR-20b modulates VEGF expression by targeting HIF-1 alpha and STAT3 in MCF-7 breast cancer cells.

2010

MicroRNAs (miRNAs) are small non-coding RNAs that regulate the expression of different genes, including genes involved in cancer progression. A functional link between hypoxia, a key feature of the tumor microenvironment, and miRNA expression has been documented. We investigated whether and how miR-20b can regulate the expression of vascular endothelial growth factor (VEGF) in MCF-7 breast cancer cells under normoxic and hypoxia-mimicking conditions (CoCl(2) exposure). Using immunoblotting, ELISA, and quantitative real-time PCR, we demonstrated that miR-20b decreased VEGF protein levels at 4 and 24 h following CoCl(2) treatment, and VEGF mRNA at 4 h of treatment. In addition, miR-20b reduce…

STAT3 Transcription FactorVascular Endothelial Growth Factor ATime FactorsPhysiologySettore MED/06 - Oncologia MedicaClinical BiochemistryDown-RegulationBreast NeoplasmsBiologyTransfectionchemistry.chemical_compoundmir20b VEGFCell Line TumormicroRNAHumansSTAT3Promoter Regions GeneticG alpha subunitRegulation of gene expressionTumor microenvironmentBinding SitesCell BiologyTransfectionCobaltHypoxia-Inducible Factor 1 alpha SubunitMolecular biologyCell HypoxiaVascular endothelial growth factorGene Expression Regulation NeoplasticMicroRNAsHIF1Achemistrybiology.proteinFemaleRNA InterferenceSignal TransductionJournal of cellular physiology
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The interleukin-22/STAT3 pathway potentiates expression of inducible nitric-oxide synthase in human colon carcinoma cells.

2007

Inducible nitric-oxide synthase (iNOS) has been identified as a marker and mediator of disease in human colonic inflammation and carcinogenesis. Accordingly, identification of mediators that trigger iNOS in colon carcinoma/epithelial cells is an important topic of current research. Here we demonstrate that interleukin (IL)-22, a newly described member of the IL-10 cytokine family, potently synergizes with interferon (IFN)-gamma for iNOS expression in human DLD-1 colon carcinoma cells. Detection of both IL-22 receptor chains and STAT3 phosphorylation proved robust IL-22 responsiveness of these cells. Short interfering RNA technology identified STAT3 as being crucial for up-regulation of iNOS…

STAT3 Transcription Factormedicine.medical_treatmentNitric Oxide Synthase Type IIBiologymedicine.disease_causeBiochemistryGene Expression Regulation EnzymologicInterleukin 22InterferonmedicineHumansRNA MessengerRNA NeoplasmSTAT3Promoter Regions GeneticMolecular BiologyInflammationInterleukinsNF-kappa BInterleukinCell BiologyTransfectionReceptors InterleukinMolecular biologyNeoplasm ProteinsGene Expression Regulation NeoplasticCytokineSTAT1 Transcription FactorColonic Neoplasmsbiology.proteinCancer researchCytokinesIntercellular Signaling Peptides and ProteinsTumor necrosis factor alphaImmunotherapyCaco-2 CellsCarcinogenesismedicine.drugSignal TransductionThe Journal of biological chemistry
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PHD3 regulates EGFR internalization and signalling in tumours

2014

Tumours exploit their hypoxic microenvironment to induce a more aggressive phenotype, while curtailing the growth-inhibitory effects of hypoxia through mechanisms that are poorly understood. The prolyl hydroxylase PHD3 is regulated by hypoxia and plays an important role in tumour progression. Here we identify PHD3 as a central regulator of epidermal growth factor receptor (EGFR) activity through the control of EGFR internalization to restrain tumour growth. PHD3 controls EGFR activity by acting as a scaffolding protein that associates with the endocytic adaptor Eps15 and promotes the internalization of EGFR. In consequence, loss of PHD3 in tumour cells suppresses EGFR internalization and hy…

Scaffold proteinmedia_common.quotation_subjectEndocytic cycleRegulatorGeneral Physics and AstronomyGeneral Biochemistry Genetics and Molecular BiologyHypoxia-Inducible Factor-Proline DioxygenasesCell Line TumorNeoplasmsmedicineHumansEpidermal growth factor receptorInternalizationmedia_commonCell ProliferationMultidisciplinarybiologyCell growthChemistryGeneral ChemistryHypoxia (medical)EndocytosisCell biologyErbB ReceptorsGene Expression Regulation NeoplasticAdaptor Proteins Vesicular TransportSignallingbiology.proteinmedicine.symptomProtein BindingSignal Transduction
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Oxidative stress in environmental-induced carcinogenesis.

2009

Reactive oxygen species (ROS) are the more abundant free radicals in nature and have been related with a number of tissue/organ injuries induced by xenobiotics, ischemia, activation of leucocytes, UV exposition, etc. Oxidative stress is caused by an imbalance between ROS production and a biological system's ability to readily detoxify these reactive intermediates or easily repair the resulting damage. Thus, oxidative stress is accepted as a critical pathophysiological mechanism in different frequent human pathologies, including cancer. In fact ROS can cause protein, lipid, and DNA damage, and malignant tumors often show increased levels of DNA base oxidation and mutations. Different lifesty…

SenescenceAgingDNA damageHealth Toxicology and MutagenesisInflammationOxidative phosphorylationBiologymedicine.disease_causeModels BiologicalNeoplasmsGeneticsmedicineAnimalsHumansObesityLife StyleCarcinogenchemistry.chemical_classificationReactive oxygen speciesCarcinogens EnvironmentalOxidative StressCell Transformation NeoplasticBiochemistrychemistryCancer researchmedicine.symptomCarcinogenesisReactive Oxygen SpeciesOxidative stressMutation research
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Is chlamydial heat shock protein 60 a risk factor for oncogenesis?

2004

Heat shock protein 60 (HSP60) plays an important role in the protein folding of prokaryotic and eukaryotic cells. Most of the papers published on chlamydial HSP60 concern its role in immune response during infection. In the last decade, exposure to Chlamydia trachomatis has been consistently associated with the development of cervical and ovarian cancer. Moreover, it has been suggested that chlamydial HSP60 may have an anti- apoptotic effect during persistent infection. We hypothesize that the accumulation of exogenous chlamydial HSP60 in the cytoplasm of actively replicating eukaryotic cells may interfere with the regulation of the apoptotic pathway. The concomitant expression of viral onc…

Senescencechlamydia hsp60Genital Neoplasms Femalechemical and pharmacologic phenomenaApoptosisChlamydia trachomatisBiologymedicine.disease_causeCellular and Molecular NeuroscienceImmune systemBacterial ProteinsRisk FactorsHeat shock proteinmedicineHumansNeoplastic transformationMolecular BiologyPharmacologyCell BiologyChaperonin 60Chlamydia InfectionsCell biologyCell Transformation NeoplasticApoptosisImmunologyMolecular MedicineHSP60FemaleCarcinogenesisChlamydia trachomatis
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Cytochemical and molecular analyses on mitochondria of immortalized and neoplastic epithelial cells of the human breast after cadmium treatments

2008

Settore BIO/06 - Anatomia Comparata E Citologiamitochondria neoplastic cells human breast cadmium
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Expression of Cyclooxygenase-1 and Cyclooxygenase-2 in normal and pathological human oral mucosa

2011

Abstract: Cyclooxigenase (COX) is the rate-limiting enzyme for the conversion of arachidonic acid (AA) to prostaglandins (PGs). Two isoforms of COX have been identified: COX-1 is constitutively expressed in many cells and is involved in cell homeostasis, angiogenesis and cell-cell signalling; COX-2 is not expressed in normal condition however it is strongly expressed in inflammation. The oral cavity is costantly exposed to physical and chemical trauma that could lead to mucosal reactions such as hyperplasia, dysplasia and cancer. Early diagnosis is the most important issue to address for a positive outcome of oral cancer; therefore it would be useful to identify molecular markers whose expr…

Settore BIO/17 - IstologiaPathologymedicine.medical_specialtyHistologyAngiogenesiscarcinoma.Settore MED/29 - Chirurgia MaxillofaccialePathology and Forensic MedicinedysplasiaSettore MED/28 - Malattie OdontostomatologichemedicineCarcinomaHumanslcsh:QH573-671Oral mucosahuman oral mucosaNeoplasm StagingMouth neoplasmbiologyReverse Transcriptase Polymerase Chain Reactionlcsh:CytologyMouth MucosahyperplasiaCancerGeneral MedicineHyperplasiamedicine.diseaseImmunohistochemistryGene Expression Regulation Neoplasticmedicine.anatomical_structurecyclooxigenasesCyclooxygenase 2DysplasiaCyclooxygenase 1biology.proteinMouth NeoplasmsCyclooxygenasecyclooxigenases human oral mucosa hyperplasia dysplasia carcinomaPrecancerous Conditions
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