Search results for "Reverse transcriptase"

showing 10 items of 715 documents

Sodium butyrate induces apoptosis in human hepatoma cells by a mitochondria/caspase pathway, associated with degradation of beta-catenin, pRb and Bcl…

2004

Butyrate can promote programmed cell death in a number of tumour cells in vitro. This paper provides evidence that butyrate induces apoptosis in human hepatoma HuH-6 and HepG2 cells but is ineffective in Chang liver cells, an immortalised non-tumour cell line. In both HuH-6 and HepG2 cells, apoptosis appeared after a lag period of approximately 16 h and increased rapidly during the second day of treatment. In particular, the effect was stronger in HuH-6 cells, which were, therefore, chosen for ascertaining the mechanism of butyrate action. In HuH-6 cells, beta-catenin seemed to exert an important protective role against apoptosis, since pretreatment with beta-catenin antisense ODN reduced t…

Cancer ResearchProgrammed cell deathbeta-CateninCarcinoma HepatocellularBlotting Westernbcl-X ProteinCaspase 3Bcl-xLApoptosisButyrateCell LineMembrane Potentialschemistry.chemical_compoundSettore BIO/10 - BiochimicaCyclin DCyclinsCyclin EHumansCaspasebeta CateninbiologyReverse Transcriptase Polymerase Chain ReactionCytochrome cLiver NeoplasmsSodium butyrateMolecular biologyButyratesCytoskeletal ProteinspRbOncologychemistryProto-Oncogene Proteins c-bcl-2ApoptosisCaspasesbiology.proteinTrans-ActivatorsPoly(ADP-ribose) PolymerasesEuropean journal of cancer (Oxford, England : 1990)
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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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MYCN and survivin cooperatively contribute to malignant transformation of fibroblasts

2013

The oncogenes MYCN and survivin (BIRC5) maintain aggressiveness of diverse cancers including sarcomas. To investigate whether these oncogenes cooperate in initial malignant transformation, we transduced them into Rat-1 fibroblasts. Indeed, survivin enhanced MYCN-driven contact-uninhibited and anchorage-independent growth in vitro. Importantly, upon subcutaneous transplantation into mice, cells overexpressing both instead of either one of the oncogenes generated tumors with shortened latency, marked anaplasia and an increased proliferation-to-apoptosis ratio resulting in accelerated growth. Mechanistically, the increased tumorigenicity was associated with an enhanced Warburg effect and a hyp…

Cancer ResearchSurvivinBlotting WesternApoptosisBiologyReal-Time Polymerase Chain ReactionN-Myc Proto-Oncogene ProteinInhibitor of Apoptosis ProteinsMalignant transformationImmunoenzyme TechniquesMiceAdenosine TriphosphateSurvivinmedicineAnimalsHumansLactic AcidRNA MessengerneoplasmsAnaplasiaCells CulturedCell ProliferationHomeodomain ProteinsOncogene ProteinsN-Myc Proto-Oncogene ProteinReverse Transcriptase Polymerase Chain ReactionCell growthNuclear ProteinsGeneral MedicineFibroblastsWarburg effectCell HypoxiaRatsTransplantationCell Transformation NeoplasticGlucoseHypoxia-inducible factorsCancer researchmedicine.symptomGlycolysisCarcinogenesis
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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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Bovine seminal ribonuclease is cytotoxic for both malignant and normal telomerase-positive cells

2005

Bovine seminal-ribonuclease (BS-RNase) is a member of the 'ribonucleases with special biological actions' family since it possesses specific anti-tumour, anti-spermatogenic and embryotoxic activities and exerts an immunosuppressive effect on T lymphocytes. In previous studies it was demonstrated that BS-RNase induced apoptosis in proliferating, malignant and normal cells and that telomerase activity loss also caused apoptotic death in neoplastic cells. Since an obvious relationship between cell proliferation and telomerase activity exists, the aim of this work was to study if the pro-apoptotic cytotoxic action exerted by BS-RNase on proliferating malignant cells (HT29) and proliferating nor…

Cancer ResearchTelomeraseTime FactorsT-LymphocytesCellular differentiationCytotoxicityBlotting WesternDown-RegulationTetrazolium SaltsAntineoplastic AgentsApoptosisEnzyme-Linked Immunosorbent AssayBiologyHT29 CellsCell Line TumorEndoribonucleasesAnimalsHumansCytotoxic T cellTelomerase reverse transcriptaseLymphocytesRNA MessengerTelomeraseBovine seminal-ribonuclease; Cytotoxicity; HTR; Nucleolar localization; TelomeraseCell ProliferationReverse Transcriptase Polymerase Chain ReactionCell growthCell DifferentiationCell cycleNucleolar localizationMolecular biologyThiazolesBovine seminal-ribonucleaseMicroscopy FluorescenceOncologyCell cultureLeukocytes MononuclearMicroscopy Electron ScanningRNACattleHTRCell NucleolusImmunosuppressive Agents
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Ganciclovir-induced apoptosis in HSV-1 thymidine kinase expressing cells: critical role of DNA breaks, Bcl-2 decline and caspase-9 activation.

2002

Although ganciclovir (GCV) is most often used in suicide anticancer gene therapy, the mechanism of GCV-induced cell killing and apoptosis is not fully understood. We analysed the mechanism of apoptosis triggered by GCV using a model system of CHO cells stably transfected with HSV-1 thymidine kinase (HSVtk). GCV-induced apoptosis is due to incorporation of the drug into DNA resulting in replication-dependent formation of DNA double-strand breaks and, at later stages, S and G2/M arrest. GCV-provoked DNA instability was likely to be responsible for the observed initial decline in Bcl-2 level and caspase-9/-3 activation. Further decline in the Bcl-2 level was due to cleavage of the protein by c…

Cancer ResearchTime FactorsvirusesPoly ADP ribose polymeraseApoptosisCytochrome c GroupCHO CellsHerpesvirus 1 HumanTransfectionThymidine KinaseCricetinaeGeneticsAnimalsfas ReceptorMolecular BiologyGanciclovirbiologyReverse Transcriptase Polymerase Chain ReactionCytochrome cCell CycleTransfectionSuicide geneFas receptorMolecular biologyCaspase 9Enzyme ActivationGene Expression Regulation NeoplasticCell killingProto-Oncogene Proteins c-bcl-2ApoptosisThymidine kinaseCaspasesbiology.proteinPoly(ADP-ribose) PolymerasesDNA DamageOncogene
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High frequency of a non-functional TAP1/LMP2 promoter polymorphism in human tumors

2002

The Tap1 and Tap2 genes encoding for a heterodimeric peptide transporter play a key role in antigen processing and presentation. The TAP complex mediates the transport of peptides generated by the IFN-gamma-inducible proteasome subunits LMP2, 7 and 10 from the cytosol into the endoplasmic reticulum (ER), where they bind to MHC class I molecules. In contrast to the frequent polymorphisms within the rat Tap genes which exert functional differences, polymorphic regions within the human Tap genes have been demonstrated, but not systematically analyzed in terms of their functional significance. Both the Tap1 and Lmp2 genes are transcribed from a bidirectional intergenic promoter which is regulat…

Cancer ResearchTransfectionViral Matrix ProteinsIntergenic regionGene FrequencyGenotypeMHC class ITumor Cells CulturedAnimalsHumansRNA MessengerATP Binding Cassette Transporter Subfamily B Member 2Promoter Regions GeneticCarcinoma Renal CellMelanomaGeneGeneticsPolymorphism GeneticbiologyReverse Transcriptase Polymerase Chain ReactionAntigen processingEndoplasmic reticulumMolecular biologyGene Expression Regulation NeoplasticOncologyCOS Cellsbiology.proteinTAP2ATP-Binding Cassette TransportersTAP1International Journal of Oncology
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The p53 Tumor Suppressor Network Is a Key Responder to Microenvironmental Components of Chronic Inflammatory Stress

2005

Abstract Activation of the p53 network plays a central role in the inflammatory stress response associated with ulcerative colitis and may modulate cancer risk in patients afflicted with this chronic disease. Here, we describe the gene expression profiles associated with four microenvironmental components of the inflammatory response (NO•, H2O2, DNA replication arrest, and hypoxia) that result in p53 stabilization and activation. Isogenic HCT116 and HCT116 TP53−/− colon cancer cells were exposed to the NO• donor Sper/NO, H2O2, hypoxia, or hydroxyurea, and their mRNA was analyzed using oligonucleotide microarrays. Overall, 1,396 genes changed in a p53-dependent manner (P < 0.001), wit…

Cancer ResearchTumor suppressor geneColorectal cancerInflammationBiologymedicine.disease_causeArticleGene expressionmedicineHumansNitric Oxide DonorsInflammationReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingCell CycleHydrogen PeroxideCell cycleHypoxia (medical)Flow CytometryHCT116 Cellsmedicine.diseaseCell HypoxiaGene expression profilingOxidative StressOncologyImmunologyNitrogen OxidesSpermineTumor Suppressor Protein p53medicine.symptomOxidative stressCancer Research
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Analysis of Antiproliferative and Chemosensitizing Effects of Sunitinib on Human Esophagogastric Cancer Cells: Synergistic Interaction With Vandetani…

2009

The receptor tyrosine kinases (RTKs), epidermal growth factor receptor (EGFR) and vascular endothelial growth factor receptor 1-3 (VEGFR1-3), are frequently expressed in gastric cancer and are putative therapeutic targets in this disease. We have investigated the anti-proliferative and chemosensitizing properties of the multitargeted small-molecule RTK inhibitors sunitinib and vandetanib in a panel of 4 human gastric and esophageal cancer cell lines. In the 1st instance, the expression of potential targets of these small-molecule inhibitors was examined by reverse transcriptase-polymerase chain reaction, western blotting, and flow cytometry. EGFR mRNA and protein was detected in all cases, …

Cancer ResearchUmbilical VeinsIndolesEsophageal NeoplasmsApoptosisVandetanibTyrosine-kinase inhibitorReceptor tyrosine kinasechemistry.chemical_compoundPiperidinesSunitinibMedicineDrug InteractionsEpidermal growth factor receptorPhosphorylationCells CulturedbiologySunitinibReverse Transcriptase Polymerase Chain ReactionDrug SynergismFlow CytometryErbB ReceptorsOncologyPhosphorylationDrug Therapy Combinationmedicine.drugSignal Transductionmedicine.medical_specialtymedicine.drug_classBlotting WesternAntineoplastic AgentsStomach NeoplasmsInternal medicineHumansPyrrolesPropidium iodideRNA MessengerProtein Kinase InhibitorsCell ProliferationVascular Endothelial Growth Factor Receptor-1business.industryCancermedicine.diseaseVascular Endothelial Growth Factor Receptor-3Vascular Endothelial Growth Factor Receptor-2EndocrinologychemistryCancer researchbiology.proteinQuinazolinesEndothelium VascularbusinessProto-Oncogene Proteins c-akt
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