Search results for " tumor suppressor"

showing 10 items of 64 documents

p53 as the main traffic controller of the cell signaling network

2010

Among different pathological conditions that affect human beings, cancer has received a great deal of attention primarily because it leads to significant morbidity and mortality. This is essentially due to increasing world-wide incidence of this disease and the inability to discover the cause and molecular mechanisms by which normal human cells acquire the characteristics that define cancer cells. Since the discovery of p53 over a quarter of a century ago, it is now recognized that virtually all cell fate pathways of live cells and the decision to die are under the control of p53. Such extensive involvement indicates that p53 protein is acting as a major traffic controller in the cell signa…

Cell signalingSettore MED/06 - Oncologia MedicaApoptosisDiseaseCell fate determinationBiologyNeoplasmsmedicineApoptosis; Cellular Senescence; Gene Expression Regulation Neoplastic; Humans; Mutation; Neoplasms; Polymorphism Genetic; Signal Transduction; Tumor Suppressor Protein p53HumansCellular SenescencePolymorphism GeneticCancerApoptosiCell cyclemedicine.diseaseCell biologyGene Expression Regulation NeoplasticThe Hallmarks of CancerApoptosisCancer cellMutationNeoplasmTumor Suppressor Protein p53HumanSignal Transduction
researchProduct

ENO1 gene product binds to the c-myc promoter and acts as a transcriptional repressor: relationship with Myc promoter-binding protein 1 (MBP-1).

2000

The Myc promoter-binding protein-1 (MBP-1) is a 37-38 kDa protein that binds to the c-myc P2 promoter and negatively regulates transcription of the protooncogene. MBP-1 cDNA shares 97% similarity with the cDNA encoding the glycolytic enzyme alpha-enolase and both genes have been mapped to the same region of human chromosome 1, suggesting the hypothesis that the two proteins might be encoded by the same gene. We show here data indicating that a 37 kDa protein is alternatively translated from the full-length alpha-enolase mRNA. This shorter form of alpha-enolase is able to bind the MBP-1 consensus sequence and to downregulate expression of a luciferase reporter gene under the control of the c…

CytoplasmTranscriptional repressionRecombinant Fusion ProteinsBiophysicsEnolaseCodon InitiatorDown-RegulationBiologyAlternative translationResponse ElementsTransfectionBiochemistryCell LineGene productHSPA4Proto-Oncogene Proteins c-mycStructural BiologyHSPA2GeneticsBiomarkers TumorE2F1AnimalsHumansSOCS6Genes Tumor SuppressorDNA bindingPromoter Regions GeneticMolecular BiologyYY1Tumor Suppressor ProteinsNuclear ProteinsCell BiologyDNAMolecular biologyGPS2Neoplasm ProteinsDNA-Binding ProteinsMolecular WeightRepressor ProteinsAlternative SplicingGATAD2BChromosomes Human Pair 1Phosphopyruvate HydrataseProtein BiosynthesisPeptidesProtein BindingFEBS letters
researchProduct

A loop involving NRF2, miR‐29b‐1‐5p and AKT, regulates cell fate of MDA‐MB‐231 triple‐negative breast cancer cells

2019

The present study shows that nuclear factor erythroid 2-related factor 2 (NRF2) and miR-29b-1-5p are two opposite forces which could regulate the fate of MDA-MB-231 cells, the most studied triple-negative breast cancer (TNBC) cell line. We show that NRF2 activation stimulates cell growth and markedly reduces reactive oxygen species (ROS) generation, whereas miR-29b-1-5p overexpression increases ROS generation and reduces cell proliferation. Moreover, NRF2 downregulates miR-29b-1-5p expression, whereas miR-29b-1-5p overexpression decreases p-AKT and p-NRF2. Furthermore, miR-29b-1-5p overexpression induces both inhibition of DNA N-methyltransferases (DNMT1, DNMT3A, and DNMT3B) expression and …

DNA (Cytosine-5-)-Methyltransferase 10301 basic medicineNF-E2-Related Factor 2PhysiologyClinical BiochemistryTriple Negative Breast NeoplasmsAKT DNMTs miR‐29b‐1‐5p NRF2 parthenolide tumor suppressor genesCell fate determinationenvironment and public healthDNA Methyltransferase 3A03 medical and health scienceschemistry.chemical_compound0302 clinical medicineSettore BIO/10 - BiochimicaCell Line TumorCyclin D2HumansParthenolideDNA (Cytosine-5-)-MethyltransferasesProtein kinase BTriple-negative breast cancerCell Proliferationchemistry.chemical_classificationReactive oxygen speciesCell growthTumor Suppressor ProteinsCell BiologyDNA Methylationrespiratory systemCell biologyGene Expression Regulation NeoplasticMicroRNAs030104 developmental biologychemistryCell culture030220 oncology & carcinogenesisDNMT1FemaleReactive Oxygen SpeciesProto-Oncogene Proteins c-aktSesquiterpenesSignal TransductionJournal of Cellular Physiology
researchProduct

Tumor suppression inDrosophila is causally related to the function of thelethal(2)tumorous imaginal discs gene, adnaJ homolog

1995

The Drosophila melanogaster tumor suppressor gene lethal(2)tumorous imaginal discs (l(2)tid) causes in homozygotes malignant growth of cells of the imaginal discs and the death of the mutant larvae at the time of puparium formation. We describe the molecular cloning of the l(2)tid+ gene and its temporal expression pattern in the wild-type and mutant alleles. Germ line rescue of the tumor phenotype was achieved with a 7.0 kb Hindlll-fragment derived from the polytene chromosome band 59F5. The l(2)tid+ gene spans approximately 2.5 kb of genomic DNA. The protein coding region, 1,696 bps long, is divided by an intron into two exons. The predicted Tid56 protein contains 518 amino acids and posse…

DNA ComplementarySaccharomyces cerevisiae ProteinsTumor suppressor geneMolecular Sequence DataMutantGenes InsectSaccharomyces cerevisiaeAnimals Genetically ModifiedFungal ProteinsMitochondrial ProteinsSpecies SpecificityEscherichia coliGeneticsAnimalsDrosophila ProteinsHumansGenes Tumor SuppressorAmino Acid SequenceCloning MolecularGeneAllelesHeat-Shock ProteinsPolytene chromosome bandBase SequenceSequence Homology Amino AcidbiologyEscherichia coli ProteinsPupaChromosome MappingExonsNeoplasms ExperimentalCell BiologyHSP40 Heat-Shock Proteinsbiology.organism_classificationMolecular biologyImaginal discDrosophila melanogasterLarvaDNAJA2Drosophila melanogasterSequence AlignmentDrosophila ProteinDevelopmental BiologyDevelopmental Genetics
researchProduct

Cloning, structure, cellular localization, and possible function of the tumor suppressor gene lethal(3)malignant blood neoplasm-1 of Drosophila melan…

1994

The tumor suppressor gene, lethal(3)malignant blood neoplasm-1+, of Drosophila melanogaster is required for the differentiation of the phagocytic blood-cell type, the plasmatocyte. In the homozygously mutated state it causes the malignant transformation of these blood cells. We present here the cloning, sequencing, structure, and expression of the l(3)mbn-1+ gene during development. The cloned gene was identified by germ-line transformation, generation of revertants, and the detection of the corresponding mRNA in blood cells and other tissues. Homologies of the G-S-rich C-terminus of the putative MBN83 protein to human cytokeratins K1, K10, and mouse loricrin were found. The structure and p…

DNA ComplementaryTumor suppressor geneMolecular Sequence DataMalignant transformationGene expressionAnimalsGenes Tumor SuppressorAmino Acid SequenceRNA MessengerCloning MolecularMolecular BiologyGeneCellular localizationAllelesCloningBlood CellsbiologyBase SequenceChromosome MappingCell Biologybiology.organism_classificationMolecular biologyCell Transformation NeoplasticDrosophila melanogasterLoricrinDrosophila melanogasterDevelopmental BiologyDevelopmental biology
researchProduct

Mitochondrial localization and temporal expression of the Drosophila melanogaster DnaJ homologous tumor suppressor Tid50

1998

The Drosophila melanogaster tumor suppressor gene lethal(2)tumorous imaginal discs (tid) was identified as a homolog of all dnaJ-like genes known to date which have been well preserved in evolution. Homozygous D. melanogaster l(2)tid mutants l(2)tid1, l(2)tid2 and l(2)tid3 are characterized by neoplastic transformation of the adult integumental primordia, the imaginal discs, and the death at the time of puparium formation. The first part of this study is concerned with the identification and subcellular localization of the l(2)tid-encoded protein, Tid50. The second part examines its tissue specific expression during wild-type development and in tumorous imaginal discs. To specify the functi…

Embryo NonmammalianTumor suppressor geneMutantGenes InsectCell FractionationBiochemistryCell LineMitochondrial ProteinsMelanogasterAnimalsDrosophila ProteinsGenes Tumor SuppressorNeoplastic transformationRNA MessengerGeneHeat-Shock ProteinsbiologyPupaGene Expression Regulation DevelopmentalRNANeoplasms ExperimentalSequence Analysis DNAOriginal ArticlesCell BiologyHSP40 Heat-Shock Proteinsbiology.organism_classificationMolecular biologyMitochondriaGene Expression Regulation NeoplasticImaginal discDrosophila melanogasterOrgan SpecificityLarvaRabbitsDrosophila melanogasterCell Stress & Chaperones
researchProduct

A temperature-sensitive brain tumor suppressor mutation of Drosophila melanogaster: Developmental studies and molecular localization of the gene

1993

The recessive-lethal, temperature-sensitive (ts) mutation of the tumor suppressor gene lethal(3)malignant brain tumor (l(3)mbt) causes in a single step the malignant transformation of the adult optic neuroblasts and ganglion mother cells in the larval brain at the restrictive temperature of 29 degrees C. The transformed cells are differentiation-incompetent and grow autonomously in a lethal and invasive fashion in situ in the brain as well as after transplantation in vivo into wild-type adult hosts. The imaginal discs show epithelial overgrowth. At the permissive temperature of 22 degrees C development is completely normal. The ts-period of gene activity responsible for 100% brain tumor sup…

EmbryologyHot TemperatureTumor suppressor geneBiologymedicine.disease_causeMalignant transformationmedicineAnimalsGenes Tumor SuppressorGeneSuppressor mutationGeneticsMutationBrain NeoplasmsStem CellsOptic Lobe NonmammalianChromosome Mappingbiology.organism_classificationCell biologyTransplantationImaginal discDrosophila melanogasterGangliaGenes LethalDrosophila melanogasterDevelopmental BiologyMechanisms of Development
researchProduct

HIF-1α induces MXI1 by alternate promoter usage in human neuroblastoma cells

2009

Adaptation to low oxygen conditions is essential for maintaining homeostasis and viability in oxygen-consuming multi-cellular tissues, including solid tumors. Central in these processes are the hypoxia-inducible transcription factors, HIF-1 and HIF-2, controlling genes involved in e.g. glucose metabolism and neovascularization. Tumor hypoxia and HIF expression have also been associated with a dedifferentiated phenotype and increased aggressiveness. In this report we show that the MAX interactor-1 (MXI1) gene is directly regulated by HIF proteins in neuroblastoma and breast cancer cells. HIF-binding and transactivation were detected within MXI1 gene regulatory sequences in the vicinity of th…

Gene isoformGenes mycBreast NeoplasmsBiologyTransfectionNeuroblastomaTransactivationCell Line TumorNeuroblastomaBasic Helix-Loop-Helix Transcription FactorsmedicineHumansGenes Tumor SuppressorRNA Small InterferingPromoter Regions GeneticGeneTranscription factorOligonucleotide Array Sequence AnalysisBase SequenceTumor hypoxiaTumor Suppressor ProteinsCell BiologyHypoxia-Inducible Factor 1 alpha Subunitmedicine.diseaseCell HypoxiaUp-RegulationGene Expression Regulation NeoplasticHIF1ARegulatory sequenceCancer researchFemaleExperimental Cell Research
researchProduct

The von Hippel-Lindau tumor suppressor gene

1997

Abstract The von Hippel-Lindau (VHL) disease is an inherited tumor susceptibility syndrome featuring a high variety of benign and malignant tumors. The gene has been localized and cloned at 3p25-26. Recent functional analysis defined the VHL gene product as an inhibitor of the transcription elongation process. Its possible involvement in the vascularization process may explain the histologic features of VHL tumors providing insight into basic mechanism of tumorigenesis. Direct genetic testing is available for patients affected with VHL. Seventy to eighty percent of the germline mutations expected could be detected. As first geno/phenotype correlations have been established, we are now begin…

GeneticsCancer Researchendocrine system diseasesmedicine.diagnostic_testTumor suppressor geneBiologyurologic and male genital diseasesmedicine.diseasemedicine.disease_causePhenotypefemale genital diseases and pregnancy complicationsGermline mutationVon Hippel–Lindau tumor suppressorGeneticsmedicineCancer researchbiology.proteinVon Hippel–Lindau diseaseCarcinogenesisMolecular BiologyGeneGenetic testingCancer Genetics and Cytogenetics
researchProduct

Genetic and molecular analysis of six tumor suppressor genes in Drosophila melanogaster

1990

Six Drosophila melanogaster tumor suppressor genes causing malignant or benign tumors in specific cell types are described. The wild-type alleles of these genes are instrumental in the differentiation of particular cell types. In the homozygous state, recessive mutations in the genes interrupt the differentiation of the cells and thus cause their uncontrolled, autonomous, lethal proliferation. The tumors show all major characteristics of malignant and benign neoplastic growth. Genomic sequences of four of the genes have been identified and are currently being characterized. ImagesFIGURE 1.FIGURE 2.FIGURE 2.

GeneticsCell typebiologyHealth Toxicology and MutagenesisRestriction MappingPublic Health Environmental and Occupational HealthNeoplastic growthNeoplasms Experimentalbiology.organism_classificationMolecular analysislaw.inventionMolecular and Cellular Aspects of Transformation and DifferentiationRestriction mapDrosophila melanogasterlawSuppressorAnimalsGenes LethalGenes Tumor SuppressorDrosophila melanogasterAlleleGeneEnvironmental Health Perspectives
researchProduct