Search results for "Tumor suppressor"

showing 10 items of 401 documents

MGMT: Key node in the battle against genotoxicity, carcinogenicity and apoptosis induced by alkylating agents

2007

O(6)-methylguanine-DNA methyltransferase (MGMT) plays a crucial role in the defense against alkylating agents that generate, among other lesions, O(6)-alkylguanine in DNA (collectively termed O(6)-alkylating agents [O(6)AA]). The defense is highly important, since O(6)AA are common environmental carcinogens, are formed endogenously during normal cellular metabolism and possibly inflammation, and are being used in cancer therapy. O(6)AA induced DNA damage is subject to repair, which is executed by MGMT, AlkB homologous proteins (ABH) and base excision repair (BER). Although this review focuses on MGMT, the mechanism of repair by ABH and BER will also be discussed. Experimental systems, in wh…

Alkylating AgentsMethyltransferaseAlkylationDNA RepairDNA repairDNA damageGene ExpressionApoptosisIn Vitro TechniquesBiologyDNA Mismatch RepairModels BiologicalBiochemistryNecrosisO(6)-Methylguanine-DNA MethyltransferaseNeoplasmsAnimalsHumansDNA Modification MethylasesneoplasmsMolecular BiologyCarcinogenChromosome AberrationsGeneticsTumor Suppressor ProteinsO-6-methylguanine-DNA methyltransferaseDNACell BiologyBase excision repairdigestive system diseasesDNA Repair EnzymesMutationCancer researchDNA mismatch repairSister Chromatid ExchangeDNA DamageAlkyltransferaseDNA Repair
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Primary mouse fibroblasts deficient for c-Fos, p53 or for both proteins are hypersensitive to UV light and alkylating agent-induced chromosomal break…

2000

The important regulatory proteins, c-Fos and p53 are induced by exposure of cells to a variety of DNA damaging agents. To investigate their role in cellular defense against genotoxic compounds, we comparatively analysed chromosomal aberrations and apoptosis induced by ultraviolet (UV-C) light and the potent alkylating agent methyl methanesulfonate (MMS) in primary diploid mouse fibroblasts knockout for either c-Fos or p53, or double knockout for both genes. We show that c-Fos and p53 deficient fibroblasts are more sensitive than the corresponding wild-type cells as to the induction of chromosomal aberrations and apoptosis. Double knockout fibroblasts lacking both c-Fos and p53 are viable an…

Alkylating AgentsUltraviolet RaysDNA repairDNA damageHealth Toxicology and MutagenesisDrug ResistanceMutagenesis (molecular biology technique)ApoptosisBiologyRadiation ToleranceCell LineMicechemistry.chemical_compoundGeneticsAnimalsMolecular BiologyGene knockoutChromosome AberrationsMice KnockoutGenes fosFibroblastsCell cycleGenes p53Molecular biologyMethyl methanesulfonatechemistryApoptosisCell cultureTumor Suppressor Protein p53Proto-Oncogene Proteins c-fosDNA DamageMutation Research/Fundamental and Molecular Mechanisms of Mutagenesis
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Cellular stress induces cap-independent alpha-enolase/MBP-1 translation.

2015

AbstractMyc promoter-binding protein-1 (MBP-1) is a shorter protein variant of the glycolytic enzyme alpha-enolase. Although several lines of evidence indicate that MBP-1 acts as a tumor suppressor, the cellular mechanisms and signaling pathways underlying MBP-1 expression still remain largely elusive. To dissect these pathways, we used the SkBr3 breast cancer cell line and non-tumorigenic HEK293T cells ectopically overexpressing alpha-enolase/MBP-1. Here, we demonstrate that induced cell stresses promote MBP-1 expression through the AKT/PERK/eIF2α signaling axis. Our results contribute to shedding light on the molecular mechanisms underlying MBP-1 expression in non-tumorigenic and cancer c…

Alpha-enolaseCellEukaryotic Initiation Factor-2Alternative translationBiochemistryeIF-2 KinaseBreast cancerHEK293 CellStructural BiologyProtein IsoformsbiologyMedicine (all)Translation (biology)Recombinant ProteinEndoplasmic Reticulum StressRecombinant ProteinsNeoplasm ProteinsDNA-Binding ProteinsGene Expression Regulation Neoplasticmedicine.anatomical_structureFemaleSignal transductionMyc promoter-binding protein-1Breast NeoplasmHumanSignal TransductionCell SurvivalDNA-Binding ProteinRecombinant Fusion ProteinsBiophysicsBreast NeoplasmsNeoplasm ProteinGeneticCell Line TumorEndoplasmic reticulum streGeneticsmedicineBiomarkers TumorHumansGene SilencingMolecular BiologyProtein kinase BTumor Suppressor ProteinTumor Suppressor ProteinsHEK 293 cellsProtein IsoformCell BiologySettore BIO/18 - GeneticaHEK293 CellsBiophysicGene Expression RegulationPhosphopyruvate HydrataseCancer cellbiology.proteinUnfolded protein responseCancer researchProto-Oncogene Proteins c-aktRecombinant Fusion ProteinFEBS letters
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Induction of apoptosis in human retinoblastoma cells by topoisomerase inhibitors

1998

PURPOSE:To examine the apoptotic effect induced in human retinoblastoma Y79 cells by camptothecin, etoposide, and amsacrine, to examine the effect of these drugs on the expression of many apoptosis-related modulators, and to test the antiapoptotic effect exerted by insulin-like growth factor-I (IGF-I). METHODS:Morphologic features of apoptosis were demonstrated using acridine orange- ethidium bromide staining and electron microscopy. DNA fragmentation was determined by means of an in situ cell detection procedure (TdT-dUTP terminal nick-end labeling [TUNEL]) or by electrophoresis on agarose gels and was quantified by enzyme-linked immunosorbent assay. The expression of apoptosis-related mod…

AmsacrineCyclin-Dependent Kinase Inhibitor p21topoisomeraseCell SurvivalRetinal NeoplasmsRetinoblastomaApoptosisDNA NeoplasmInsulin-Like Growth Factor Binding Protein 3DNA Topoisomerases Type IProto-Oncogene Proteins c-bcl-2CyclinsProto-Oncogene ProteinsDactinomycinTumor Cells CulturedHumansCamptothecinCycloheximideEnzyme InhibitorsTopoisomerase I InhibitorsTumor Suppressor Protein p53DNA DamageEtoposidebcl-2-Associated X Protein
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The lipoprotein receptor LRP1 modulates sphingosine-1-phosphate signaling and is essential for vascular development

2014

Low density lipoprotein receptor-related protein 1 (LRP1) is indispensable for embryonic development. Comparing different genetically engineered mouse models, we found that expression of Lrp1 is essential in the embryo proper. Loss of LRP1 leads to lethal vascular defects with lack of proper investment with mural cells of both large and small vessels. We further demonstrate that LRP1 modulates Gi-dependent sphingosine-1-phosphate (S1P) signaling and integrates S1P and PDGF-BB signaling pathways, which are both crucial for mural cell recruitment, via its intracellular domain. Loss of LRP1 leads to a lack of S1P-dependent inhibition of RAC1 and loss of constraint of PDGF-BB-induced cell migra…

AngiogenesisBlotting WesternBecaplerminEmbryonic DevelopmentNeovascularization PhysiologicRAC1BiologyReal-Time Polymerase Chain ReactionMural cellchemistry.chemical_compoundMiceCell MovementSphingosineHuman Umbilical Vein Endothelial CellsAnimalsHumansSphingosine-1-phosphateMolecular BiologyResearch ArticlesIn Situ HybridizationSphingosineTumor Suppressor ProteinsCell migrationCell BiologyProto-Oncogene Proteins c-sisLRP1ImmunohistochemistryCell biologyMicroscopy ElectronchemistryReceptors LDLLow-density lipoproteinSignal transductionLysophospholipidsGenetic EngineeringLow Density Lipoprotein Receptor-Related Protein-1Developmental BiologySignal Transduction
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The transmembrane receptor Uncoordinated5 (Unc5) is essential for heart lumen formation in Drosophila melanogaster

2011

AbstractTransport of liquids or gases in biological tubes is fundamental for many physiological processes. Our knowledge on how tubular organs are formed during organogenesis and tissue remodeling has increased dramatically during the last decade. Studies on different animal systems have helped to unravel some of the molecular mechanisms underlying tubulogenesis. Tube architecture varies dramatically in different organs and different species, ranging from tubes formed by several cells constituting the cross section, tubes formed by single cells wrapping an internal luminal space or tubes that are formed within a cell. Some tubes display branching whereas others remain linear without interse…

AngiogenesisLumen (anatomy)Receptors Cell SurfaceOrganogenesisLumen formationBiologyLigandsUnc5AnimalsDrosophila ProteinsDrosophila heart morphogenesisMyocytes CardiacNerve Growth FactorsReceptorMolecular BiologyCardiogenesisTumor Suppressor ProteinsHeartCell BiologyAnatomyNetrin-1Tubulogenesisbiology.organism_classificationTransmembrane proteinCell biologyDrosophila melanogasterNetrinBSignal transductionDrosophila melanogasterNetrin ReceptorsDrosophila ProteinDevelopmental BiologyDevelopmental Biology
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Resistance of p53 knockout cells to doxorubicin is related to reduced formation of DNA strand breaks rather than impaired apoptotic signaling

2003

The anthracycline doxorubicin (adriamycin) is an important chemotherapeutic agent used in the treatment of solid epithelial and mesenchymal tumors as well as leukemias. A variety of mechanisms has been proposed to be involved in doxorubicin-induced cytotoxicity such as DNA intercalation, oxidative stress, DNA strand breakage by inhibition of topoisomerase II, activation of death receptors, and altered p53 expression. Concerning doxorubicin resistance and p53 status data reported are contradictory. Here, we show that mouse fibroblasts deficient in p53 (p53(-/-)) are more resistant to doxorubicin than p53 wild-type (p53 wt) cells. This is in contrast to other genotoxic agents (UV-light, alkyl…

AnthracyclineApoptosisIn Vitro TechniquesBiochemistryCell LineMicemedicineAnimalsTopoisomerase II InhibitorsDoxorubicinMolecular BiologyEtoposideMice KnockoutbiologyTopoisomeraseCell BiologyFas receptorMolecular biologyDoxorubicinDrug Resistance NeoplasmCell cultureApoptosisCancer researchbiology.proteinTumor Suppressor Protein p53Topoisomerase-II InhibitorDNA DamageSignal Transductionmedicine.drugDNA Repair
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Targeting p53, hdm2, and CD19: vaccination and immunologic strategies.

2000

Peptides presented by class I major histocompatibility complex (MHC) molecules and derived from normal self-proteins that are expressed at elevated levels by cells from a variety of human (Hu) malignancies provide, in theory, potential target antigens for a broad-spectrum, cytotoxic T lymphocyte (CTL)-based immunotherapy of cancer and hematologic malignancies. However, as such tumor- and leukemia-associated self-proteins are also expressed at low levels in some types of normal tissues, such as thymus, spleen and lymphohemopoietic cells, these self-MHC-self-peptide complexes may also represent thymic and/or peripheral tolerogens, thereby preventing immune responses. This is particularly true…

Antigen presentationAntigens CD19chemical and pharmacologic phenomenaMice TransgenicMajor histocompatibility complexEpitopeMiceImmune systemAntigenNeoplasmsProto-Oncogene ProteinsCytotoxic T cellAnimalsHumansAvidityTransplantationAntigen PresentationbiologyHistocompatibility Antigens Class IVaccinationNuclear ProteinsProto-Oncogene Proteins c-mdm2HematologyCTL*Immunologybiology.proteinTumor Suppressor Protein p53T-Lymphocytes CytotoxicBone marrow transplantation
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Resveratrol modulates the levels of microRNAs targeting genes encoding tumor-suppressors and effectors of TGFbeta signaling pathway in SW480 cells.

2010

International audience; Resveratrol (trans-3,4',5-trihydroxystilbene) is a natural antioxidant with cardiovascular and cancer preventive properties that is currently at the stage of pre-clinical studies for human cancer prevention. Beside its known effects on protein coding genes, one possible mechanism for resveratrol protective activities is by modulating the levels of non-coding RNAs. Here, we analyzed the effects of resveratrol on microRNA populations in human SW480 colon cancer cells. We establish that resveratrol treatment decreases the levels of several oncogenic microRNAs targeting genes encoding Dicer1, a cytoplasmic RNase III producing mature microRNAs from their immediate precurs…

Antineoplastic AgentsSmad ProteinsResveratrolBiochemistryAntioxidantsArticleTransforming Growth Factor beta1chemistry.chemical_compoundTGFβTransforming Growth Factor betaCell Line TumormicroRNAStilbenesPTENHumansRibonuclease III[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyPharmacologyOncogene ProteinsbiologyEffectorTumor Suppressor ProteinsTransforming growth factor betaMolecular biologyColon cancer; microRNAs; miR-663; Resveratrol; SW480 cells; TGFβmiR-663Cell biologyColon cancerMicroRNAsSW480 cellschemistryResveratrolbiology.proteinSignal transductionTransforming growth factorSignal Transduction
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Enhancement of cytotoxicity of artemisinins toward cancer cells by ferrous iron

2004

Abstract Iron(II) heme-mediated activation of the peroxide bond of artemisinins is thought to generate the radical oxygen species responsible for their antimalarial activity. We analyzed the role of ferrous iron in the cytotoxicity of artemisinins toward tumor cells. Iron(II)–glycine sulfate (Ferrosanol) and transferrin increased the cytotoxicity of free artesunate, artesunate microencapsulated in maltosyl-β-cyclodextrin, and artemisinin toward CCRF-CEM leukemia and U373 astrocytoma cells 1.5- to 10.3-fold compared with that of artemisinins applied without iron. Growth inhibition by artesunate and ferrous iron correlated with induction of apoptosis. Cell cycle perturbations by artesunate an…

ArtemisininsIronPopulationTransferrin receptorBiochemistryFerrousInhibitory Concentration 50chemistry.chemical_compoundAntigens CDCell Line TumorNeoplasmsPhysiology (medical)Receptors TransferrinHumansFerrous CompoundsRNA MessengereducationCell Proliferationchemistry.chemical_classificationeducation.field_of_studybiologyMolecular biologyArtemisininsAntigens Differentiation B-LymphocyteGene Expression RegulationBiochemistrychemistryTransferrinArtesunateCancer cellbiology.proteinTumor Suppressor Protein p53CeruloplasminFree Radical Biology and Medicine
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