Search results for "Neoplastic"

showing 10 items of 2901 documents

Updated Field Synopsis and Systematic Meta-Analyses of Genetic Association Studies in Cutaneous Melanoma: The MelGene Database

2015

We updated a field synopsis of genetic associations of cutaneous melanoma (CM) by systematically retrieving and combining data from all studies in the field published as of August 31, 2013. Data were available from 197 studies, which included 83,343 CM cases and 187,809 controls and reported on 1,126 polymorphisms in 289 different genes. Random-effects meta-analyses of 81 eligible polymorphisms evaluated in4 data sets confirmed 20 single-nucleotide polymorphisms across 10 loci (TYR, AFG3L1P, CDK10, MYH7B, SLC45A2, MTAP, ATM, CLPTM1L, FTO, and CASP8) that have previously been published with genome-wide significant evidence for association (P5 × 10(-8)) with CM risk, with certain variants pos…

SLC45A2Skin NeoplasmsLocus (genetics)DermatologyPolymorphism Single NucleotideBiochemistryLinkage DisequilibriumGermlineStatistical significanceDatabases GeneticOdds RatioHumansGenetic Predisposition to DiseaseMelanomaGeneMolecular BiologyGerm-Line MutationGenetic associationGeneticsbiologyChromosome MappingGenetic VariationCell BiologyGene Expression Regulation NeoplasticCutaneous melanomabiology.proteinGenome-Wide Association StudyJournal of Investigative Dermatology
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MiR-29b antagonizes the pro-inflammatory tumor-promoting activity of multiple myeloma-educated dendritic cells

2017

Dendritic cells (DCs) have a key role in regulating tumor immunity, tumor cell growth and drug resistance. We hypothesized that multiple myeloma (MM) cells might recruit and reprogram DCs to a tumor-permissive phenotype by changes within their microRNA (miRNA) network. By analyzing six different miRNA-profiling data sets, miR-29b was identified as the only miRNA upregulated in normal mature DCs and significantly downregulated in tumor-associated DCs. This finding was validated in primary DCs co-cultured in vitro with MM cell lines and in primary bone marrow DCs from MM patients. In DCs co-cultured with MM cells, enforced expression of miR-29b counteracted pro-inflammatory pathways, includin…

STAT3 Transcription Factor0301 basic medicineCancer Researchdendritic cellDown-RegulationInflammationMice SCIDBiologyMice03 medical and health sciences0302 clinical medicineDownregulation and upregulationBone MarrowCell Line Tumorhemic and lymphatic diseasesmicroRNAmedicineAnimalsHumanstumor immunologyMultiple myelomaCell ProliferationInflammationmicroRNA.Cell growthNF-kappa BDendritic CellsHematologySTAT3 Transcription Factormedicine.diseaseNFKB1Up-RegulationGene Expression Regulation Neoplasticmultiple myelomaMicroRNAs030104 developmental biologymedicine.anatomical_structureOncologyCancer researchOriginal ArticleFemaleBone marrowTh17medicine.symptom030215 immunology
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Parthenolide sensitizes hepatocellular carcinoma cells to trail by inducing the expression of death receptors through inhibition of STAT3 activation

2011

This article shows that HepG2, Hep3B, and SK-Hep1 cells, three lines of human hepatocellular carcinoma (HCC) cells, are resistant to apoptosis induced by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). Parthenolide, a sesquiterpene lactone found in European feverfew, has been shown to exert both anti-inflammatory and anti-cancer activities. This article demonstrates that co-treatment with parthenolide and TRAIL-induced apoptosis with synergistic interactions in the three lines of HCC cells. In order to explain these effects we ascertained that parthenolide increased either at protein or mRNA level the total content of death receptors TRAIL-R1 and -R2 as well as their surfac…

STAT3 Transcription FactorCarcinoma HepatocellularPhysiologyClinical BiochemistryCellDown-RegulationTRAILApoptosisPharmacologyParthenolideSTAT3TNF-Related Apoptosis-Inducing Ligandchemistry.chemical_compoundSettore BIO/10 - BiochimicamedicineHumansParthenolidePhosphorylationReceptorSTAT3CaspaseJanus KinasesbiologyLiver NeoplasmsProto-Oncogene Proteins c-mdm2Hep G2 CellsReceptors Death DomainCell BiologyapoptosiEnzyme ActivationGene Expression Regulation Neoplasticmedicine.anatomical_structurechemistryCell cultureApoptosisCaspasesbiology.proteinSTAT proteinDrug Screening Assays AntitumorTumor Suppressor Protein p53SesquiterpenesJournal of Cellular Physiology
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Signaling molecules: the pathogenic role of the IL-6/STAT-3 trans signaling pathway in intestinal inflammation and in colonic cancer.

2008

Although the precise etiology of inflammatory bowel diseases (IBD) still remains unclear, considerable progress has been made in the identification of novel signal transduction pathways that elucidate the immunopathogenesis involved in the perpetuation of the inflammatory process. As both ulcerative colitis and Crohn's disease are associated with an increased risk for developing colorectal cancer (CRC) and precancerous dysplastic epithelial changes, further studies have concentrated on finding a common signaling pathway that could serve as a mechanistic link between inflammation and associated colonic cancer in IBD. This review presents the current data concerning the pathogenic role of the…

STAT3 Transcription FactorCell signalingColorectal cancerClinical BiochemistryAnti-Inflammatory AgentsInflammationAntineoplastic AgentsDiseaseSuppressor of cytokine signallingDrug DiscoverymedicineAnimalsHumansAutocrine signallingPharmacologybusiness.industryInterleukin-6medicine.diseaseInflammatory Bowel DiseasesUlcerative colitisdigestive system diseasesCell Transformation NeoplasticColonic NeoplasmsCancer researchMolecular Medicinemedicine.symptomSignal transductionbusinessSignal TransductionCurrent drug targets
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The antitumor activities of curcumin and its isoxazole analogue are not affected by multiple gene expression changes in an MDR model of the MCF-7 bre…

2007

We examined the effects of curcumin and of its isoxazole analogue MR 39 in the MCF-7 breast cancer cell line and in its multidrug-resistant (MDR) variant MCF-7R. In comparison with MCF-7, MCF-7R lacks estrogen receptor alpha (ERalpha) and overexpressess P-glycoprotein (P-gp), different IAPs (inhibitory of apoptosis proteins) and COX-2. Through analyses of the effects on cell proliferation, cycling and death, we have observed that the antitumor activity of curcumin and of the more potent (approximately two-fold) MR 39 is at least equal in the MDR cell line compared to the parental MCF-7. Similar results were observed also in an MDR variant of HL-60 leukemia. RT-PCR evaluations performed in M…

STAT3 Transcription FactorCurcuminGene ExpressionEstrogen receptorBreast NeoplasmsBiologyPharmacologycurcumin isoxazole derivative multidrug resistance P-glycoprotein estrogen receptor inhibitory of apoptosis proteinschemistry.chemical_compoundCell Line TumorGeneticsHumansskin and connective tissue diseasesCell ProliferationP-glycoproteinCell DeathCell growthCell CycleTranscription Factor RelAGeneral MedicineCell cycleAntineoplastic Agents PhytogenicDrug Resistance MultipleMultiple drug resistancechemistryMCF-7Drug Resistance Neoplasmbiology.proteinCurcuminFemaleEstrogen receptor alpha
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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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