Search results for "prime"

showing 10 items of 853 documents

Deficient expression of components of the MHC class I antigen processing machinery in human cervical carcinoma.

2001

In cervical carcinomas abnormalities in the MHC class I surface expression are a frequent event, which are often associated with the deficient expression of the peptide transporter subunit TAP1 thereby resulting in impaired T cell response. In order to understand the role of other components of the MHC class I antigen processing machinery (APM) in the immune escape, 16 surgically removed primary cervical carcinoma lesions were analyzed for their mRNA expression of the heterodimeric peptide transporter TAP, the constitutive and interferon (IFN)-gamma inducible proteasome subunits and their activators PA28alpha/beta, various chaperones as well as MHC class I antigens. High expression levels o…

Cancer ResearchAntigen presentationBlotting WesternDown-RegulationGene ExpressionGenes MHC Class IUterine Cervical NeoplasmsHuman leukocyte antigenBiologyInterferon-gammaInterferonMHC class ImedicineBiomarkers TumorTumor Cells CulturedHumansRNA MessengerCells CulturedDNA PrimersAntigen PresentationAntigen processingMHC class I antigenReverse Transcriptase Polymerase Chain ReactionHistocompatibility Antigens Class ITransporter associated with antigen processingNeoplasm ProteinsPhenotypeOncologyImmunologyCancer researchbiology.proteinFemaleTAP1medicine.drugInternational journal of oncology
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Role of glutathione in the induction of apoptosis and c-fos and c-jun mRNAs by oxidative stress in tumor cells.

2003

We have used two tumor cell clones (B9 and G2), derived from the methylcholanthrene-induced murine fibrosarcoma GR9 and normal BALB/c3T3 fibroblasts, to study the ability of t-BOOH derived reactive oxygen radicals to induce oxidative stress, apoptosis and c-fos and c-jun mRNA transcription. These clones differ in terms of their major histocompatibility complex (MHC) (H-2) class I genes expression, their tumor induction and metastatic potential and their reduced glutathione (GSH) levels. Incubation of both cell clones in the presence of t-BOOH results in the increase of 8-oxo-2'-deoxyguanosine (8-oxo-dG) and malondialdehyde and the decrease of GSH. The xenobiotic also induces the transcripti…

Cancer ResearchBALB 3T3 CellsTranscription GeneticProto-Oncogene Proteins c-junFibrosarcomaCellApoptosisBiologymedicine.disease_causeAntioxidantsSuperoxide dismutasechemistry.chemical_compoundMicetert-ButylhydroperoxideCell CloneMalondialdehydemedicineTumor Cells CulturedAnimalsRNA MessengerDNA Primerschemistry.chemical_classificationReactive oxygen speciesReverse Transcriptase Polymerase Chain Reactionc-junHistocompatibility Antigens Class IDeoxyguanosineGlutathioneFibroblastsMolecular biologyGlutathioneOxidative Stressmedicine.anatomical_structureOncologychemistryGene Expression RegulationApoptosis8-Hydroxy-2'-Deoxyguanosinebiology.proteinReactive Oxygen SpeciesProto-Oncogene Proteins c-fosOxidative stressCancer letters
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Regulation of human inducible nitric oxide synthase expression by an upstream open reading frame.

2019

Abstract The human inducible nitric oxide synthase (iNOS) gene contains an upstream open reading frame (uORF) in its 5′-untranslated region (5′-UTR) implying a translational regulation of iNOS expression. Transfection experiments in human DLD-1 cells revealed that the uORF although translatable seems not to inhibit the translation start at the bona fide ATG. Our data clearly show that human iNOS translation is cap-dependent and that the 5′-UTR of the iNOS mRNA contains no internal ribosome entry site. Translation of the bona fide coding sequence is most likely mediated by a leaky scanning mechanism. The 5′-UTR is encoded by exon 1 and exon 2 of the iNOS gene with the uORF stop codon located…

Cancer ResearchFive prime untranslated regionPhysiologyClinical BiochemistryDown-RegulationNitric Oxide Synthase Type IILeaky scanningBiochemistryExonOpen Reading FramesCell Line TumorUpstream open reading frameTranslational regulationCoding regionHumansAmino Acid SequenceBase SequenceChemistryIntronExonsIntronsCell biologyNonsense Mediated mRNA DecayInternal ribosome entry siteGene Expression RegulationMutationTrans-ActivatorsRNA HelicasesNitric oxide : biology and chemistry
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Antitumor effect of B16 melanoma cells genetically modified with the angiogenesis inhibitor rnasin.

2001

The growth of new blood vessels is an essential condition for the development of tumors with a diameter greater than 1-2 mm and also for their metastatic dissemination. RNasin, the placental ribonuclease inhibitor, is known to have antiangiogenic activity through the inhibition of angiogenin and basic fibroblast growth factor. Nevertheless, the administration of the recombinant form of a protein poses several limitations; as a result, we have studied the antitumor effect of RNasin in a murine gene therapy model. RNasin cDNA was subcloned into the pcDNA3 expression vector, and the resulting recombinant plasmid was used to transfect the B16 murine melanoma cell line. An RNasin inverted constr…

Cancer ResearchLung NeoplasmsAngiogeninTranscription GeneticGenetic enhancementCellBasic fibroblast growth factorGenetic VectorsMelanoma ExperimentalGene ExpressionAngiogenesis InhibitorsTransfectionNeovascularizationImmunoenzyme Techniqueschemistry.chemical_compoundMiceRibonucleasesmedicineTumor Cells CulturedAnimalsHumansRNA MessengerEnzyme InhibitorsMolecular BiologyDNA PrimersNeovascularization PathologicReverse Transcriptase Polymerase Chain ReactionMelanomaGenetic Therapymedicine.diseaseAngiogenesis inhibitormedicine.anatomical_structurechemistryCell cultureCancer researchMolecular Medicinemedicine.symptomPlacental HormonesCell DivisionCancer gene therapy
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Enhanced expression of ELAM-1 on endothelium of renal cell carcinoma compared to the corresponding normal renal tissue

1999

Abstract Renal cell carcinoma (RCC) has been shown to respond to an immunological therapy with tumor infiltrating lymphocytes (TIL), which accumulate in RCC at a higher density than in normal renal tissue, suggesting that there is selective tumor invasion. Since invasion of TIL into the malignant tissue is mediated by adhesion molecules, we examined the different expression of the adhesion molecule endothelial-leukocyte-adhesion-molecule-1 (ELAM-1) on endothelial cells of RCC versus normal renal tissue. For a specific quantification, the level of ELAM-1 mRNA was investigated by both semi-quantitative reverse transcription–polymerase chain reaction (RT–PCR) and Northern blot analysis and ref…

Cancer ResearchPathologymedicine.medical_specialtyEndotheliumBiologyKidneyurologic and male genital diseasesImmunoenzyme TechniquesRenal cell carcinomaGene expressionmedicineCarcinomaHumansRNA MessengerNorthern blotCarcinoma Renal CellDNA PrimersKidneyReverse Transcriptase Polymerase Chain ReactionTumor-infiltrating lymphocytesCell adhesion moleculeBlotting Northernmedicine.diseaseKidney Neoplasmsmedicine.anatomical_structureOncologyCancer researchEndothelium VascularE-SelectinCancer Letters
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Identification and validation of novel ERBB2 (HER2, NEU) targets including genes involved in angiogenesis.

2005

V-erb-b2 erythroblastic leukemia viral oncogene homolog 2 (ERBB2; synonyms HER2, NEU) encodes a transmembrane glycoprotein with tyrosine kinase-specific activity that acts as a major switch in different signal-transduction processes. ERBB2 amplification and overexpression have been found in a number of human cancers, including breast, ovary and kidney carcinoma. Our aim was to detect ERBB2-regulated target genes that contribute to its tumorigenic effect on a genomewide scale. The differential gene expression profile of ERBB2-transfected and wild-type mouse fibroblasts was monitored employing DNA microarrays. Regulated expression of selected genes was verified by RT-PCR and validated by West…

Cancer ResearchReceptor ErbB-2Blotting WesternViral OncogeneDown-RegulationComputational biologyBiologymedicine.disease_causeTransfectionGenomeMiceGene expressionmedicineAnimalsHumansskin and connective tissue diseasesGeneDNA PrimersGlycoproteinsOligonucleotide Array Sequence AnalysisGeneticsRegulation of gene expressionGenomeNeovascularization PathologicReverse Transcriptase Polymerase Chain ReactionFibroblastsGenes erbB-2Up-RegulationGene expression profilingGene Expression Regulation NeoplasticCell Transformation NeoplasticOncologyNIH 3T3 CellsDNA microarrayCarcinogenesisSignal TransductionInternational journal of cancer
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Regulation of CD1d expression by murine tumor cells: escape from immunosurveillance or alternate target molecules?

2002

alpha beta+ TCR T cells recognize peptide fragments displayed by MHC-class I or -class II molecules. Recently, additional mechanisms of antigen recognition by T cells have been identified, including CD1-mediated presentation of nonpeptide antigens. Only a limited number of CD1 antigens is retained in the mouse, i.e., the group II CD1 antigens, which are split into CD1D1 and CD1d2. Several T cell subsets have been shown to interact with murine CD1 antigens, including NK cells or "natural T cells" with the invariant V alpha 14 J alpha 281 TCR chain. Even if TAP defects may prevent classical endogenous antigen presentation in tumor cell lines, antigen presentation via CD1 is still functional. …

Cancer ResearchT cellAntigen presentationCD1chemical and pharmacologic phenomenaBiologyNatural killer cellAntigens CD1Immunoenzyme TechniquesInterferon-gammaMiceNK-92Monitoring ImmunologicmedicineCytotoxic T cellAnimalsRNA MessengerAntigen-presenting cellCells CulturedDNA PrimersMice Inbred BALB CReverse Transcriptase Polymerase Chain ReactionAntibodies MonoclonalGranulocyte-Macrophage Colony-Stimulating Factorhemic and immune systemsNeoplasms ExperimentalCytotoxicity Tests ImmunologicFlow CytometryCell biologyGene Expression Regulation NeoplasticKiller Cells NaturalMice Inbred C57BLmedicine.anatomical_structureOncologyCD1DImmunologybiology.proteinCytokinesAntigens CD1dInternational journal of cancer
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Differential MHC class II component expression in HPV-positive cervical cancer cells: implication for immune surveillance.

2005

Effective eradication of human papillomavirus (HPV)-positive tumors may require CD8+ and CD4+ T-cell-mediated immune responses. Ectopic expression of MHC class II surface molecules has been described in the context of cervical cancer, but coexpression with other components of the MHC class II antigen presentation pathway has not been addressed. We have evaluated the MHC class II antigen presentation pathway in malignant squamous epithelium of HPV+ cervical cancer lesions by in situ costaining HLA-DR with CLIP or DMA/DMB. Cervical cancer cells exhibit 3 MHC class II phenotypes: (i) DR+/CLIP+ or DM+; (ii) DR+/CLIP- or DM-; and (iii) DR-/CLIP+ or DM+. The identical profile has been identified …

Cancer ResearchT cellT-LymphocytesFluorescent Antibody TechniqueUterine Cervical NeoplasmsEnzyme-Linked Immunosorbent AssayMHC class II antigenInterferon-gammaAntigenMHC class ImedicineHumansPapillomaviridaeDNA PrimersMHC class IIbiologyBase SequenceAntigen processingReverse Transcriptase Polymerase Chain ReactionHistocompatibility Antigens Class IIMHC restrictionmedicine.anatomical_structureOncologyImmunologybiology.proteinFemaleCD8International journal of cancer
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Nuclear insulin receptor substrate 1 interacts with estrogen receptor alpha at ERE promoters.

2004

Insulin receptor substrate 1 (IRS-1) is a major signaling molecule activated by the insulin and insulin-like growth factor I receptors. Recent data obtained in different cell models suggested that in addition to its conventional role as a cytoplasmic signal transducer, IRS-1 has a function in the nuclear compartment. However, the role of nuclear IRS-1 in breast cancer has never been addressed. Here we report that in estrogen receptor alpha (ERalpha)-positive MCF-7 cells, (1) a fraction of IRS-1 was translocated to the nucleus upon 17-beta-estradiol (E2) treatment; (2) E2-dependent nuclear translocation of IRS-1 was blocked with the antiestrogen ICI 182,780; (3) nuclear IRS-1 colocalized and…

Cancer Researchmedicine.medical_specialtyTranscription Geneticmedicine.medical_treatmentBlotting WesternEstrogen receptorBiologyInsulin-like growth factorInternal medicineCell Line TumorGeneticsmedicineAnimalsHumansReceptorPromoter Regions GeneticMolecular BiologyNuclear receptor co-repressor 1DNA PrimersBase SequenceReverse Transcriptase Polymerase Chain ReactionEstrogen Receptor alphaPromoterAntiestrogenPhosphoproteinsPrecipitin TestsIRS1Cell biologyProtein TransportEndocrinologyNuclear receptorReceptors EstrogenInsulin Receptor Substrate ProteinsProtein BindingOncogene
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The Synthetic Cannabinoid WIN 55,212-2 Sensitizes Hepatocellular Carcinoma Cells to Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand (TRAIL)-I…

2010

In this article, we demonstrate that the synthetic cannabinoid R-(+)-(2,3-dihydro-5-methyl-3-[(4-morpholinyl)methyl]pyrol[1,2,3-de]-1,4-benzoxazin-6-yl)-(1-naphthalenyl) methanone mesylate (WIN 55,212-2) sensitizes human hepatocellular carcinoma (HCC) cells to apoptosis mediated by tumor necrosis-related apoptosis inducing ligand (TRAIL). The apoptotic mechanism induced by treatment with WIN/TRAIL combination involved the loss of the mitochondrial transmembrane potential and led to the activation of caspases. In HCC cells, WIN treatment induced the up-regulation of TRAIL death receptor DR5, an effect that seemed to be related to the increase in the level of p8 and CHOP, two factors implicat…

Carcinoma HepatocellularDNA ComplementaryMorpholinesApoptosisNaphthalenesCHOPMembrane PotentialsTNF-Related Apoptosis-Inducing LigandCell Line TumorSurvivinmedicineHumansWIN 55212-2Protein kinase BTranscription factorCaspaseDNA PrimersPharmacologybiologyCannabinoidsReverse Transcriptase Polymerase Chain ReactionLiver NeoplasmsGene AmplificationDNA NeoplasmFlow CytometryBenzoxazinesReceptors TNF-Related Apoptosis-Inducing LigandApoptosisMitochondrial MembranesImmunologybiology.proteinCancer researchMolecular MedicineTumor necrosis factor alphaTranscription Factor CHOPmedicine.drugMolecular Pharmacology
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