Search results for "Tumor suppressor"

showing 10 items of 401 documents

Selective induction of apoptosis in multidrug resistant HL60R cells by the thiazolobenzoimidazole derivative 1-(2,6-difluorophenyl)-1H,3H-thiazolo [3…

1999

We investigated the antitumour effects of 1-(2,6-difluorophenyl)-1H,3H-thiazolo [3,4-a]benzimidazole (TBZ) a new anti-HIV-1 agent, on human promyelocytic HL60 leukaemia, both a parental and a multidrug resistant form (HL60R). HL60R overexpresses P-glycoprotein and, like HL60, lacks p53 protein expression. HL60 and HL60R show similar levels of Bcl-2 protein. In contrast to the conventional chemotherapeutic agents daunorubicin, etoposide and mitoxantrone, TBZ caused equal or even greater cytotoxicity in HL60R than in HL60, and this result was associated with a more marked induction of apoptosis in the drug resistant cells. The antitumour activity of TBZ occurred in the range of concentrations…

Cancer ResearchBenzimidazoleAnti-HIV AgentsDaunorubicinHL60ApoptosisHL-60 CellsDrug resistancePharmacologychemistry.chemical_compoundmedicineHumansATP Binding Cassette Transporter Subfamily B Member 1CytotoxicityP-glycoproteinbiologyFlow CytometryVirologyDrug Resistance MultipleMultiple drug resistanceThiazolesProto-Oncogene Proteins c-bcl-2OncologychemistryDrug Resistance NeoplasmApoptosisbiology.proteinBenzimidazolesDrug Screening Assays AntitumorTumor Suppressor Protein p53medicine.drugEuropean Journal of Cancer
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Why do results conflict regarding the prognostic value of the methylation status in colon cancers? The role of the preservation method.

2012

Abstract Background In colorectal carcinoma, extensive gene promoter hypermethylation is called the CpG island methylator phenotype (CIMP). Explaining why studies on CIMP and survival yield conflicting results is essential. Most experiments to measure DNA methylation rely on the sodium bisulfite conversion of unmethylated cytosines into uracils. No study has evaluated the performance of bisulfite conversion and methylation levels from matched cryo-preserved and Formalin-Fixed Paraffin Embedded (FFPE) samples using pyrosequencing. Methods Couples of matched cryo-preserved and FFPE samples from 40 colon adenocarcinomas were analyzed. Rates of bisulfite conversion and levels of methylation of …

Cancer ResearchBisulfite sequencing[SDV.CAN]Life Sciences [q-bio]/CancerAdenocarcinomaBiologyMLH1lcsh:RC254-282[ SDV.CAN ] Life Sciences [q-bio]/Cancerchemistry.chemical_compound[SDV.CAN] Life Sciences [q-bio]/CancerPredictive Value of TestsBiomarkers TumorGeneticsHumansSulfitesDNA Modification MethylasesAdaptor Proteins Signal TransducingCryopreservationParaffin EmbeddingTumor Suppressor ProteinsNuclear ProteinsReproducibility of ResultsDNA NeoplasmMethylationDNA MethylationPrognosislcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensMolecular biologydigestive system diseasesNeoplasm ProteinsBisulfiteDNA Repair EnzymesLong Interspersed Nucleotide ElementsPhenotypeOncologyCpG sitechemistrySodium bisulfiteColonic NeoplasmsDNA methylationFeasibility StudiesPyrosequencingCpG IslandsMutL Protein Homolog 1Research Article
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Hepatitis C Virus Core Protein Inhibits Tumor Suppressor Protein Promyelocytic Leukemia Function in Human Hepatoma Cells

2005

Abstract Tumor suppressor protein promyelocytic leukemia (PML) is implicated in apoptosis regulation and antiviral response. PML localizes predominantly to PML-nuclear bodies (PML-NB), nuclear macromolecular complexes regulating tumor suppressor protein p53 activity. Consistent with the function of PML in the cellular antiviral response, PML-NBs represent preferential targets in viral infections. In the case of hepatitis C virus (HCV) infection, important characteristics are nonresponsiveness to IFN therapy and development of hepatocellular carcinoma. However, the mechanisms which lead to the development of hepatocellular carcinoma are largely unknown. Here, we show that HCV core protein lo…

Cancer ResearchCarcinoma HepatocellularTumor suppressor genevirusesApoptosisPromyelocytic Leukemia ProteinBiologyTransfectionmedicine.disease_causePromyelocytic leukemia proteinCell Line TumorCoactivatormedicineHumansProtein IsoformsPhosphorylationCell NucleusTumor Suppressor ProteinsViral Core ProteinsLiver NeoplasmsNuclear Proteinsvirus diseasesAcetylationFas receptorHepatitis Cdigestive system diseasesNeoplasm ProteinsOncologyApoptosisAcetylationbiology.proteinCancer researchPhosphorylationTumor Suppressor Protein p53CarcinogenesisTranscription FactorsCancer Research
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Differences in the mechanisms of growth control in contact-inhibited and serum-deprived human fibroblasts

1997

In the present work we studied mechanisms of growth control in contact-inhibited and serum-deprived human diploid fibroblasts. The observation that the effects on [3H]thymidine incorporation and reduction of retinoblastoma gene product-phosphorylation were additive when contact-inhibition and serum-deprivation were combined led us to the conclusion that the underlying mechanisms might be different. Both contact-inhibition and serum-deprivation led to a strong decrease of cdk4-kinase-activity and cdk2-phosphorylation at Thr 160, while the total amounts of cdk4 and cdk2 remained constant. In contact-inhibited cells, we revealed a strong protein accumulation of the cdk2-inhibitor p27 and a sli…

Cancer ResearchCell Cycle ProteinsProtein Serine-Threonine KinasesRetinoblastoma ProteinCulture Media Serum-FreeS PhaseCyclin D1CyclinsProto-Oncogene ProteinsCDC2-CDC28 KinasesGeneticsmedicineHumansCyclin D1Cyclin D3PhosphorylationCyclin D3FibroblastMolecular BiologyCyclin-Dependent Kinase Inhibitor p16CyclinbiologyCell growthTumor Suppressor ProteinsCyclin-Dependent Kinase 2Cyclin-dependent kinase 2G1 PhaseCyclin-Dependent Kinase 4FibroblastsDiploidyCyclin-Dependent KinasesCulture MediaCell biologymedicine.anatomical_structureCell culturebiology.proteinbiological phenomena cell phenomena and immunitySignal transductionMicrotubule-Associated ProteinsCell DivisionCyclin-Dependent Kinase Inhibitor p27Oncogene
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In human retinoblastoma Y79 cells okadaic acid-parthenolide co-treatment induces synergistic apoptotic effects, with PTEN as a key player.

2013

Retinoblastoma is the most common intraocular malignancy of childhood. In developing countries, treatment is limited, long-term survival rates are low and current chemotherapy causes significant morbidity to pediatric patients and significantly limits dosing. Therefore there is an urgent need to identify new therapeutic strategies to improve the clinical outcome of patients with retinoblastoma. here, we investigated the effects of two natural compounds okadaic acid (OKa) and parthenolide (PN) on human retinoblastoma Y79 cells. For the first time we showed that OKa/PN combination at subtoxic doses induces potent synergistic apoptotic effects accompanied by lowering in p-akt levels, increasin…

Cancer ResearchCell SurvivalGene ExpressionAntineoplastic AgentsApoptosisBiologychemistry.chemical_compoundSettore BIO/10 - BiochimicaCell Line TumorOkadaic AcidmedicinePTENCytotoxic T cellHumansParthenolideViability assayProtein kinase BCell ShapePharmacologyRetinoblastomaPTEN PhosphohydrolaseRetinoblastomaDrug SynergismProto-Oncogene Proteins c-mdm2Okadaic acidmedicine.diseaseGlutathioneOxidative StressOncologychemistryApoptosisCancer researchbiology.proteinMolecular Medicineretinoblastoma Y79 cells synergistic apoptotic effects oxidative stress natural drugs PTEN/Akt/Mdm2/p53 pathway parthenolide okadaic acid.Drug Screening Assays AntitumorTumor Suppressor Protein p53Reactive Oxygen SpeciesProtein Processing Post-TranslationalProto-Oncogene Proteins c-aktSesquiterpenesResearch PaperCancer biologytherapy
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The human Lgl polarity gene, Hugl-2, induces MET and suppresses Snail tumorigenesis

2012

Lethal giant larvae proteins have key roles in regulating polarity in a variety of cell types and function as tumour suppressors. A transcriptional programme initiated by aberrant Snail expression transforms epithelial cells to potentially aggressive cancer cells. Although progress in defining the molecular determinants of this programme has been made, we have little knowledge as to how the Snail-induced phenotype can be suppressed. In our studies we identified the human lethal giant larvae homologue 2, Hugl-2, (Llgl2/Lgl2) polarity gene as downregulated by Snail. Snail binds E-boxes in the Hugl-2 promoter and represses Hugl-2 expression, whereas removal of the E-boxes releases Hugl-2 from …

Cancer ResearchCell typeMice SCIDSnailmedicine.disease_causeMiceMice Inbred NODbiology.animalChlorocebus aethiopsparasitic diseasesCell polarityGeneticsmedicineAnimalsHumansGenes Tumor SuppressorNeoplasm MetastasisMolecular BiologyTranscription factorCells CulturedRegulation of gene expressionbiologyfungiHEK 293 cellsCell PolarityHep G2 CellsAnatomyProto-Oncogene Proteins c-metXenograft Model Antitumor AssaysPhenotypeUp-RegulationCell biologyGene Expression Regulation NeoplasticCytoskeletal ProteinsCell Transformation NeoplasticHEK293 CellsCOS CellsSnail Family Transcription FactorsCarcinogenesisProtein BindingTranscription FactorsOncogene
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Detection of the DCC gene product in normal and malignant colorectal tissues and its relation to a codon 201 mutation.

1998

Protein expression of the putative tumour-suppressor gene DCC on chromosome 18q was evaluated in a panel of 16 matched colorectal cancer and normal colonic tissue samples together with DCC mRNA expression and allelic deletions (loss of heterozygosity, LOH). Determined by a polymerase chain reaction (PCR)-LOH assay, 12 of the 16 (75%) cases were informative with LOH occurring in 2 of the 12 cases. For DCC mRNA, transcripts could be detected in all analysed normal tissues (eight out of eight) by RT-PCR, whereas 6 of the 15 tumours were negative. DCC protein expression, investigated by immunohistochemistry using the monoclonal antibody 15041 A directed against the intracellular domain, was hom…

Cancer ResearchDeleted in Colorectal CancerDNA Mutational AnalysisLoss of HeterozygosityReceptors Cell SurfaceBiologymedicine.disease_causePolymerase Chain ReactionLoss of heterozygosityGene productmedicineHumansGenes Tumor SuppressorRNA MessengerRNA NeoplasmCodonGeneMessenger RNAMutationTumor Suppressor ProteinsfungiDCC ReceptorImmunohistochemistryNeoplasm ProteinsBlotting SouthernOncologyCancer researchImmunohistochemistryColorectal NeoplasmsCell Adhesion MoleculesImmunostainingResearch ArticleBritish Journal of Cancer
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Diverse roles of GSK-3: tumor promoter-tumor suppressor, target in cancer therapy.

2013

Glycogen synthase kinase-3 (GSK-3) is a critical enzyme which participates in a complex array of important cellular processes and is often involved in various human diseases. It was first characterized in rat skeletal muscle as a serine/threonine (S/T) kinase that phosphorylated and inactivated glycogen synthase (GS). GS is the last enzyme in glycogen biosynthesis . Thus the initially identified role of GSK-3 was in metabolism. However, as we will soon see, GSK-3 has many diverse functions.

Cancer ResearchENZYMECarcinogenesisCancer therapymacromolecular substancesBiologymedicine.disease_causeGSK3law.inventionGlycogen Synthase Kinase 3GeneticlawGSK-3NeoplasmsGeneticsmedicineAnimalsHumansGenes Tumor SuppressorGenes tumor suppressorMolecular BiologyGeneCarcinogenesiAnimalNeoplasms therapyMolecular medicineMetabolismCancer researchNeoplasmMolecular MedicineSuppressorCarcinogenesisGlycogenHumanAdvances in biological regulation
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Transcriptomic responses generated by hepatocarcinogens in a battery of liver-based in vitro models

2013

As the conventional approach to assess the potential of a chemical to cause cancer in humans still includes the 2-year rodent carcinogenicity bioassay, development of alternative methodologies is needed. In the present study, the transcriptomics responses following exposure to genotoxic (GTX) and non-genotoxic (NGTX) hepatocarcinogens and non-carcinogens (NC) in five liver-based in vitro models, namely conventional and epigenetically stabilized cultures of primary rat hepatocytes, the human hepatoma-derived cell lines HepaRG and HepG2 and human embryonic stem cell-derived hepatocyte-like cells, are examined. For full characterization of the systems, several bioinformatics approaches are emp…

Cancer ResearchGene Expressiongene expression profilingComputational biologyBiologyPharmacologyTranscriptomeRats Sprague-Dawley03 medical and health sciences0302 clinical medicineCell Line TumorBioassayAnimalsHumansGeneCarcinogenEmbryonic Stem Cells030304 developmental biology0303 health sciencesGene Expression ProfilingLiver Neoplasmspathwaysbased analysis liver-based in vitro modelGeneral MedicineHep G2 CellsEmbryonic stem cellIn vitro3. Good healthRatsgenotoxic carcinogens non-genotoxic carcinogensGene expression profilingLiverCell culture030220 oncology & carcinogenesisCarcinogensHepatocytesTumor Suppressor Protein p53TranscriptomeMutagens
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Down-regulation of CYLD as a trigger for NF-κB activation and a mechanism of apoptotic resistance in hepatocellular carcinoma cells

2010

The cylindromatosis gene (CYLD) was identified as a tumor suppressor gene, which is mutated in familial cylindromatosis (Brooke-Spiegler syndrome), an autosomal-dominant predisposition to multiple tumors of the skin appendages. CYLD is a deubiquitinating enzyme acting as a negative regulator of the nuclear factor κB (NF-κB) signaling pathway by removing lysine-63-linked polyubiquitin chains from NF-κB activating proteins. In order to investigate the role of CYLD in apoptotic signaling in human hepatocellular carcinoma (HCC) cells, we first studied the expression levels of CYLD in HCC tissues. CYLD expression was lower in HCC both at protein and mRNA levels compared to the surrounding non-ma…

Cancer ResearchGene knockdownTumor suppressor geneOncogeneCell cycleBiologydigestive system diseasesDeubiquitinating Enzyme CYLDOncologyCancer researchbiology.proteinTumor necrosis factor alphaEpidermal growth factor receptorSignal transductionInternational Journal of Oncology
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