Search results for "Gene Silencing"

showing 10 items of 216 documents

Hypoxia inducible factor-1alpha inactivation unveils a link between tumor cell metabolism and hypoxia-induced cell death.

2008

Hypoxia and the acquisition of a glycolytic phenotype are intrinsic features of the tumor microenvironment. The hypoxia inducible factor-1alpha (HIF-1alpha) pathway is activated under hypoxic conditions and orchestrates a complex transcriptional program that enhances cell survival. Although the consequences of HIF-1alpha inactivation in cancer cells have been widely investigated, only a few studies have addressed the role of HIF-1alpha in the survival of cancer cells endowed with different glycolytic capacities. In this study, we investigated this aspect in ovarian cancer cells. Hypoxia-induced toxicity was increased in highly glycolytic cells compared with poorly glycolytic cells; it was a…

Programmed cell deathMice SCIDBiologyPathology and Forensic MedicineMiceCell Line TumormedicineAnimalsHumansGene SilencingRNA Small InterferingCell ProliferationOvarian NeoplasmsTumor microenvironmentCell DeathCell growthLentivirusHypoxia (medical)Hypoxia-Inducible Factor 1 alpha SubunitCell HypoxiaCell biologyPhenotypeHypoxia-inducible factorsApoptosisCell cultureCancer cellFemalemedicine.symptomRegular ArticlesThe American journal of pathology
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ROS-Dependent ER Stress and Autophagy Mediate the Anti-Tumor Effects of Tributyltin (IV) Ferulate in Colon Cancer Cells

2020

Organotin compounds represent potential cancer therapeutics due to their pro-apoptotic action. We recently synthesized the novel organotin ferulic acid derivative tributyltin (IV) ferulate (TBT-F) and demonstrated that it displays anti-tumor properties in colon cancer cells related with autophagic cell death. The purpose of the present study was to elucidate the mechanism of TBT-F action in colon cancer cells. We specifically show that TBT-F-dependent autophagy is determined by a rapid generation of reactive oxygen species (ROS) and correlated with endoplasmic reticulum (ER) stress. TBT-F evoked nuclear factor erythroid-2 related factor 2 (Nrf2)-mediated antioxidant response and Nrf2 silenc…

Programmed cell deathNF-E2-Related Factor 2Glucose-regulated proteinApoptosismedicine.disease_causeArticleCatalysisInorganic Chemistrylcsh:ChemistrySettore BIO/10 - BiochimicaAutophagyTumor Cells CulturedmedicineHumansGene silencingoxidative stressPhysical and Theoretical ChemistryEndoplasmic Reticulum Chaperone BiPMolecular Biologylcsh:QH301-705.5tributyltin (IV) derivativeSpectroscopyCell Proliferationoxidative strebiologyChemistryEndoplasmic reticulumOrganic ChemistryAutophagyCancerROSGeneral Medicineendoplasmic reticulum stremedicine.diseaseComputer Science ApplicationsGene Expression Regulation Neoplasticlcsh:Biology (General)lcsh:QD1-999autophagic cell deathColonic NeoplasmsUnfolded protein responseCancer researchbiology.proteinendoplasmic reticulum stressTrialkyltin CompoundsReactive Oxygen SpeciesOxidative stress
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Calpain 1 and 2 Are Required for RNA Replication of Echovirus 1▿

2007

ABSTRACT Calpains are calcium-dependent cysteine proteases that degrade cytoskeletal and cytoplasmic proteins. We have studied the role of calpains in the life cycle of human echovirus 1 (EV1). The calpain inhibitors, including calpeptin, calpain inhibitor 1, and calpain inhibitor 2 as well as calpain 1 and calpain 2 short interfering RNAs, completely blocked EV1 infection in the host cells. The effect of the inhibitors was not specific for EV1, because they also inhibited infection by other picornaviruses, namely, human parechovirus 1 and coxsackievirus B3. The importance of the calpains in EV1 infection also was supported by the fact that EV1 increased calpain activity 3 h postinfection. …

ProteasesImmunoelectron microscopyImmunologyParechovirusVirus ReplicationMicrobiologyCell LineViral entryVirologyHumansGene SilencingEnzyme InhibitorsMicroscopy ImmunoelectronMicroscopy ConfocalbiologyCalpainCytoplasmic VesiclesRNACalpainMolecular biologyCell biologyVirus-Cell InteractionsEnterovirus B HumanViral replicationCell cultureInsect ScienceCalpain-2biology.proteinRNA Viral
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Label-free quantitative proteomic profiling of colon cancer cells identifies acetyl-CoA carboxylase alpha as antitumor target of Citrus limon-derived…

2017

Abstract We have previously isolated exosome-like nanoparticles from Citrus-limon juice, able to inhibit in vitro and in vivo tumor cell growth. In order to deeply understand the mechanism underlying nanovesicle effects, we performed a proteomic profile of treated colorectal cancer cells. Among the proteins differentially expressed after nanovesicle treatment, we found a significant downregulation of the Acetyl-CoA Carboxylase 1 (ACACA) and we demonstrated that silencing ACACA in cancer cells leads to a reduction of cell growth. Our study proved that the anti-tumor effects of Citrus-limon nanovesicles is partly mediated by lipid metabolism inhibition, in particular via ACACA downregulation.…

Proteomics0301 basic medicineCitrusBiophysicsBiologyExosomesBiochemistry03 medical and health sciencesDownregulation and upregulationSettore BIO/13 - Biologia ApplicataCell Line TumorHumansGene silencingCell ProliferationLabel-free quantitative proteomic analysisACACAProteomic ProfileProteomic ProfilingCell growthCitrus-limon nanovesicleAcetyl-CoA carboxylaseLipid MetabolismColorectal cancer030104 developmental biologyBiochemistryColonic NeoplasmsCancer cellCancer researchAcetyl-CoA CarboxylaseJournal of Proteomics
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In Vitro Phenotypic, Genomic and Proteomic Characterization of a Cytokine-Resistant Murine β-TC3 Cell Line

2012

Type 1 diabetes mellitus (T1DM) is caused by the selective destruction of insulin-producing β-cells. This process is mediated by cells of the immune system through release of nitric oxide, free radicals and pro-inflammatory cytokines, which induce a complex network of intracellular signalling cascades, eventually affecting the expression of genes involved in β-cell survival. The aim of our study was to investigate possible mechanisms of resistance to cytokine-induced β-cell death. To this purpose, we created a cytokine-resistant β-cell line (β-TC3R) by chronically treating the β-TC3 murine insulinoma cell line with IL-1β + IFN-γ. β-TC3R cells exhibited higher proliferation rate and resistan…

ProteomicsAnatomy and Physiologymedicine.medical_treatmentCell Culture Techniqueslcsh:MedicineApoptosisSettore MED/13 - EndocrinologiaMiceEndocrinologyImmune PhysiologyInsulin-Secreting CellsMolecular Cell BiologySOCS3lcsh:ScienceMultidisciplinaryCell DeathDiabetes mellitus cytokines. apoptosis SUMO4 NF-kBCell CycleNF-kappa BGenomicsCell cycleImmunohistochemistryCell biologyPhenotypeCytokineMedicineCytokinesResearch ArticleProgrammed cell deathCell SurvivalImmunologyDown-RegulationBiologyAutoimmune DiseasesCell LineDownregulation and upregulationmedicineAnimalsGene SilencingBiologyCell ProliferationDiabetic EndocrinologyEndocrine PhysiologyCell growthlcsh:RCell cultureApoptosisImmune SystemClinical ImmunologyInsulinomalcsh:QPLoS ONE
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Mboat7 down-regulation by hyper-insulinemia induces fat accumulation in hepatocytes.

2020

Background: Naturally occurring variation in Membrane-bound O-acyltransferase domain-containing 7 (MBOAT7), encoding for an enzyme involved in phosphatidylinositol acyl-chain remodelling, has been associated with fatty liver and hepatic disorders. Here, we examined the relationship between hepatic Mboat7 down-regulation and fat accumulation. Methods: Hepatic MBOAT7 expression was surveyed in 119 obese individuals and in experimental models. MBOAT7 was acutely silenced by antisense oligonucleotides in C57Bl/6 mice, and by CRISPR/Cas9 in HepG2 hepatocytes. Findings: In obese individuals, hepatic MBOAT7 mRNA decreased from normal liver to steatohepatitis, independently of diabetes, inflammatio…

Research paperTGFβ Transforming Growth Factor BetaIntracellular SpaceCRISPR Clustered Regularly Interspaced Short Palindromic RepeatshHEPS Human HepatocytesMice0302 clinical medicineLPIAT1DAG Diacylglyceroli.p. Intraperitonealmedia_commonFatty AcidsGeneral Medicine3. Good health030220 oncology & carcinogenesisHOMA-IR homeostasis Model Assessment of Insulin ResistanceMPO morpholinolcsh:Medicine (General)medicine.medical_specialtyPE Phosphatidyl-EthanolamineNashGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesTNFα tumor Necrosis Factor AlphaLDL Low Density LipoproteinsHyperinsulinismNAFLDSD Standard Dietmedia_common.cataloged_instanceHumansCPT1 Carnitine Palmitoyltransferase IPhosphatidylinositolGene SilencingEuropean unionVLDL Very Low Density Lipoproteinlcsh:RhHSC Human Hepatic Stellate Cellsmedicine.diseaseLipid MetabolismOA Oleic AcidCI Confidence IntervalMboat7 Membrane bound O-acyltransferase domain containing 7MCD methionine choline deficient diet030104 developmental biologyEndocrinologychemistryCDP Cytidine-DiphosphateFOXO1 Forkhead Box protein O1NAFLD nonalcoholic fatty liver diseaseSteatohepatitisBMI Body Mass IndexCL CardiolipinAcyltransferases0301 basic medicineAlcoholic liver diseaseCXCL10 C-X-C Motif Chemokine 10lcsh:Medicinechemistry.chemical_compoundNon-alcoholic Fatty Liver DiseaseIFG Impaired Fasting GlucoseAPOB Apolipoprotein BNonalcoholic fatty liver diseasePIP Phosphatidyl-Inositol-PhosphateSteatohepatitisqRT-PCR quantitative Real Time Polymerase Chain ReactionMice Knockoutlcsh:R5-920ORO Oil Red O StainingPI PhosphatidylinositolFatty liverTM6SF2 Transmembrane 6 Superfamily Member 2PhospholipidTAG TriglyceridesNASH Nonalcoholic SteatohepatitisLipogenesisLPA Lyso-Phosphatidic AcidPhosphatidylinositolSignal TransductionPS Phosphatidyl-SerinePA Palmitic AcidALD alcoholic liver diseasePC Phosphatidylcholinei.v. IntravenousFATP1 Fatty Acid Transport Protein 1Models BiologicalInternal medicinemedicineAnimalsNonalcoholic fatty liver diseasePPARα Peroxisome Proliferator-Activated Receptor alphaObesityG3P Glyceraldehyde-3-PhosphateSREBP1c Sterol Regulatory Element-Binding Protein 1HDL High Density Lipoproteinsbusiness.industryPI3K Phosphatidylinositol 3 KinaseMembrane ProteinsNHEJ Non-Homologues End JoiningPNPLA3 Patatin-like Phospholipase Domain-containing-3MTTP Microsomal Triglyceride Transfer ProteinLPIAT1 Lysophosphatidylinositol Acyltransferase 1TMC4 Transmembrane Channel-Like 4Disease Models AnimalGene Expression RegulationHepatocytesFOXA2 Forkhead Box A2mTOR mammalian target of RapamycinSteatosisInsulin ResistancebusinessPG Phosphatidyl-GlycerolFABP1 Fatty Acid-Binding Protein 1 FAS Fatty Acid SynthaseT2DM Type 2 Diabetes MellitusEBioMedicine
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Dual-targeting siRNAs.

2010

We have developed an algorithm for the prediction of dual-targeting short interfering RNAs (siRNAs) in which both strands are deliberately designed to separately target different mRNA transcripts with complete complementarity. An advantage of this approach versus the use of two separate duplexes is that only two strands, as opposed to four, are competing for entry into the RNA-induced silencing complex. We chose to design our dual-targeting siRNAs as Dicer substrate 25/27mer siRNAs, since design features resembling pre-microRNAs (miRNAs) can be introduced for Dicer processing. Seven different dual-targeting siRNAs targeting genes that are potential targets in cancer therapy have been develo…

STAT3 Transcription FactorSmall interfering RNATranscription GeneticTrans-acting siRNAGenes mycMethodComputational biologyKidneyPolymerase Chain ReactionCell LineSuppression GeneticRNA interferencemicroRNAGene silencingHumansRNA MessengerRNA Small InterferingMolecular BiologyGeneticsGene knockdownbiologyBase SequenceRNAProtein Biosynthesisbiology.proteinProto-Oncogene Proteins c-bcl-6AlgorithmsDicerRNA (New York, N.Y.)
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Proteomic analysis reveals a role for Bcl2-associated athanogene 3 and major vault protein in resistance to apoptosis in senescent cells by regulatin…

2014

Senescence is a prominent solid tumor response to therapy in which cells avoid apoptosis and instead enter into prolonged cell cycle arrest. We applied a quantitative proteomics screen to identify signals that lead to therapy-induced senescence and discovered that Bcl2-associated athanogene 3 (Bag3) is up-regulated after adriamycin treatment in MCF7 cells. Bag3 is a member of the BAG family of co-chaperones that interacts with Hsp70. Bag3 also regulates major cell-signaling pathways. Mass spectrometry analysis of the Bag3 Complex revealed a novel interaction between Bag3 and Major Vault Protein (MVP). Silencing of Bag3 or MVP shifts the cellular response to adriamycin to favor apoptosis. We…

SenescenceProteomicsCell cycle checkpointApoptosisBreast NeoplasmsBAG3BiochemistryAnalytical ChemistryMajor vault proteinCell Line TumorGene silencingHumansMolecular BiologyCellular SenescenceAdaptor Proteins Signal TransducingVault Ribonucleoprotein ParticlesMitogen-Activated Protein Kinase 1Antibiotics AntineoplasticMitogen-Activated Protein Kinase 3biologyResearchCell biologyApoptosisDoxorubicinbiology.proteinCancer researchSignal transductionApoptosis Regulatory ProteinsCell agingSignal TransductionMolecularcellular proteomics : MCP
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Histone Variant MacroH2A1 Marks Liver Aging and Orchestrates the Escape from Senescence Induced by DNA Hypomethylation in Hepatocellular Carcinoma

2015

The epigenetic basis of age-associated progression of liver diseases towards hepatocellular carcinoma (HCC) is unclear. MacroH2A1 is a variant of histone H2A1, present in the two isoforms, with fundamental roles in cell homeostasis. MacroH2A1 is a marker of senescence associated heterochromatic foci (SAHF) and synergizes with DNA demethylating chemotherapic agent 5-aza-2'-deoxycytidine (5-aza-dC) in silencing tumor suppressor genes in human fibroblasts. We show that protein levels of macroH2A1 isoforms are increased in the livers of old rodents and humans, and in human HCC tissue. Human HCC cells overexpressing macroH2A1 escape a 5-aza-dC-induced senescent phenotype, as determined by cell p…

SenescencebiologyCell growthCell cycleBiochemistryCell biologyHistoneGeneticsbiology.proteinGene silencingEpigeneticsMolecular BiologyGeneBiotechnologyDNA hypomethylation
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Intrinsically disordered protein PID-2 modulates Z granules and is required for heritable piRNA-induced silencing in the Caenorhabditis elegans embryo

2020

Abstract In Caenorhabditis elegans, the piRNA (21U RNA) pathway is required to establish proper gene regulation and an immortal germline. To achieve this, PRG‐1‐bound 21U RNAs trigger silencing mechanisms mediated by RNA‐dependent RNA polymerase (RdRP)‐synthetized 22G RNAs. This silencing can become PRG‐1‐independent and heritable over many generations, a state termed RNA‐induced epigenetic gene silencing (RNAe). How and when RNAe is established, and how it is maintained, is not known. We show that maternally provided 21U RNAs can be sufficient for triggering RNAe in embryos. Additionally, we identify PID‐2, a protein containing intrinsically disordered regions (IDRs), as a factor required …

Small RNAPiwi-interacting RNApiRNABiologyGeneral Biochemistry Genetics and Molecular BiologyArticleEpigenesis Genetic570 Life sciences03 medical and health scienceschemistry.chemical_compound0302 clinical medicineProtein DomainsRNA polymeraseGene silencingAnimalsEpigeneticsGene SilencingRNA Small InterferingPID‐5Caenorhabditis elegansCaenorhabditis elegans ProteinsMolecular BiologyPID‐4Caenorhabditis elegans030304 developmental biologyPID‐2Regulation of gene expression0303 health sciencesGeneral Immunology and MicrobiologyGeneral NeuroscienceRNAGene Expression Regulation DevelopmentalArticlesbiology.organism_classificationRNA BiologyCell biologyIntrinsically Disordered ProteinschemistryArgonaute ProteinsZ granuleDevelopment & Differentiation030217 neurology & neurosurgeryProtein Binding570 Biowissenschaften
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