Search results for " Proliferation"

showing 10 items of 1137 documents

Micronucleus induction and cell cycle alterations produced by deoxynivalenol and its acetylated derivatives in individual and combined exposure on He…

2018

Mycotoxins are produced by a number of fungal genera spp as e.g. Aspergillus, Penicillium, Alternaria, Fusarium and Claviceps. 3-Acetyl-Deoxynivalenol (3-A-DON) and 15-Acetyl-Deoxynivalenol (15-ADON) which are produced by Fusarium, chemically belong to trichothecenes and occur in significant amounts as modified forms of deoxynivalenol (DON) in various cereal crops and processed grains. This study aims to determine the cytotoxicity, cell cycle and genotoxicity of the mycotoxins DON, 3-A-DON and 15-A-DON on HepG2 cells. Cytotoxic concentration range studied was from 100 to 3.1 μM for DON and 12.5 to 0.04 μM for 3-A-DON and 15-A-DON by the Neutral Red (NR) assay, over 24, 48 and 72 h. Potentia…

0301 basic medicineFusariumNeutral redCell SurvivalToxicologymedicine.disease_cause03 medical and health scienceschemistry.chemical_compound0404 agricultural biotechnologymedicineHumansMycotoxinCell ProliferationMicronucleus TestsbiologyCell Cyclefood and beveragesAcetylation04 agricultural and veterinary sciencesGeneral MedicineHep G2 CellsCell cyclebiology.organism_classification040401 food scienceMolecular biology030104 developmental biologychemistryPenicilliumMicronucleus testMicronucleusTrichothecenesGenotoxicityFood ScienceFood and chemical toxicology : an international journal published for the British Industrial Biological Research Association
researchProduct

Anthranilamide-based 2-phenylcyclopropane-1-carboxamides, 1,1'-biphenyl-4-carboxamides and 1,1'-biphenyl-2-carboxamides: Synthesis biological evaluat…

2017

Abstract Several anthranilamide-based 2-phenylcyclopropane-1-carboxamides 13a-f, 1,1’-biphenyl-4-carboxamides 14a-f and 1,1’-biphenyl-2-carboxamides 17a-f were obtained by a multistep procedure starting from the (1S,2S)-2-phenylcyclopropane-1-carbonyl chloride 11, the 1,1'-biphenyl-4-carbonyl chloride 12 or the 1,1'-biphenyl-2-carbonyl chloride 16 with the appropriate anthranilamide derivative 10a-f. Derivatives 13a-f, 14a-f and 17a-f showed antiproliferative activity against human leukemia K562 cells. Among these derivatives 13b, 14b and 17b exerted a particular cytotoxic effect on tumor cells. Derivative 17b showed a better antitumoral effect on K562 cells than 13b and 14b. Analyses perfo…

0301 basic medicineG2 Phase2-Phenylcyclopropane-1-carboxamides 11’-biphenyl-4-carboxamides 11’-biphenyl-2-carboxamides G2/M arrest Phospho-ATM and gH2AX increaseDNA RepairDNA repairStereochemistryAntineoplastic AgentsApoptosisChloride03 medical and health scienceschemistry.chemical_compound0302 clinical medicineSettore BIO/10 - BiochimicaDrug DiscoverymedicineCytotoxic T cellHumansortho-AminobenzoatesMode of actionCell ProliferationPharmacologyChemistryOrganic ChemistryGeneral MedicineCell Cycle CheckpointsCell cycleSettore CHIM/08 - Chimica Farmaceutica030104 developmental biologyMechanism of actionApoptosis030220 oncology & carcinogenesismedicine.symptomK562 CellsDNAmedicine.drugDNA Damage
researchProduct

Redox signaling in the gastrointestinal tract.

2017

Redox signaling regulates physiological self-renewal, proliferation, migration and differentiation in gastrointestinal epithelium by modulating Wnt/β-catenin and Notch signaling pathways mainly through NADPH oxidases (NOXs). In the intestine, intracellular and extracellular thiol redox status modulates the proliferative potential of epithelial cells. Furthermore, commensal bacteria contribute to intestine epithelial homeostasis through NOX1- and dual oxidase 2-derived reactive oxygen species (ROS). The loss of redox homeostasis is involved in the pathogenesis and development of a wide diversity of gastrointestinal disorders, such as Barrett's esophagus, esophageal adenocarcinoma, peptic ulc…

0301 basic medicineGastrointestinal DiseasesNotch signaling pathwaymedicine.disease_causeBiochemistryGastrointestinal epitheliumSuperoxide dismutase03 medical and health scienceschemistry.chemical_compoundPhysiology (medical)medicineHumansSulfhydryl CompoundsIntestinal MucosaWnt Signaling PathwayCell Proliferationchemistry.chemical_classificationReactive oxygen speciesbiologySuperoxideWnt signaling pathwayNADPH OxidasesDual oxidase 2digestive system diseasesGastrointestinal TractIntestinesOxidative Stress030104 developmental biologychemistryImmunologybiology.proteinCancer researchReactive Oxygen SpeciesOxidation-ReductionOxidative stressFree radical biologymedicine
researchProduct

ZNF518B gene up-regulation promotes dissemination of tumour cells and is governed by epigenetic mechanisms in colorectal cancer

2019

AbstractMost of colorectal cancer CRC-related death is due to metastasis and the finding of markers for prognosis of invasiveness, constitutes an appealing challenge. Here, after analysing cDNA array containing 43 tumour and 5 normal mucosa samples, we report that the expression of the ZNF518B gene as a whole and that of its two major splicing isoforms are significantly increased in tumours. The canonical isoform was also up-regulated in a patients’ cohort containing 70 tumour and 69 adjacent tissue samples. The effects of silencing ZNF518B on the phenotype of CRC cell lines were then studied. The gene does not affect cell proliferation, but plays a significant role in cell migration and in…

0301 basic medicineGene isoformEpithelial-Mesenchymal TransitionCelllcsh:MedicineBiologyArticleHistone DeacetylasesEpigenesis GeneticHistones03 medical and health sciences0302 clinical medicineCell MovementCell Line TumorGene expressionmedicineGene silencingHumansProtein IsoformsEpigeneticsNeoplasm Metastasislcsh:ScienceGeneCell ProliferationNeoplasm StagingMultidisciplinaryGene Expression Profilinglcsh:RPrognosisColorectal cancer3. Good healthDNA-Binding ProteinsGene Expression Regulation Neoplastic030104 developmental biologymedicine.anatomical_structureHistoneGene Knockdown TechniquesCancer researchbiology.proteinH3K4me3lcsh:QEpigeneticsColorectal Neoplasms030217 neurology & neurosurgeryScientific Reports
researchProduct

MiR-144 overexpression as a promising therapeutic strategy to overcome glioblastoma cell invasiveness and resistance to chemotherapy

2019

Abstract Glioblastoma (GB) is the most aggressive and common form of primary brain tumor, characterized by fast proliferation, high invasion, and resistance to current standard treatment. The average survival rate post-diagnosis is only of 14.6 months, despite the aggressive standard post-surgery treatment approaches of radiotherapy concomitant with chemotherapy with temozolomide. Altered cell metabolism has been identified as an emerging cancer hallmark, including in GB, thus offering a new target for cancer therapies. On the other hand, abnormal expression levels of miRNAs, key regulators of multiple molecular pathways, have been correlated with pathological manifestations of cancer, such…

0301 basic medicineGenetic enhancementmedicine.medical_treatmentBrain tumorAntineoplastic AgentsBiology03 medical and health sciences0302 clinical medicineDownregulation and upregulationCell MovementCell Line TumormicroRNAGeneticsmedicineHumansRNA MessengerU87Molecular BiologyGenetics (clinical)Cell ProliferationTemozolomideBrain NeoplasmsGene Expression ProfilingCancerGeneral Medicinemedicine.disease3. Good healthGene Expression Regulation NeoplasticRadiation therapyMicroRNAs030104 developmental biologyDrug Resistance Neoplasm030220 oncology & carcinogenesisCancer researchEnergy MetabolismGlioblastomamedicine.drugHuman Molecular Genetics
researchProduct

miR-22 suppresses DNA ligase III addiction in multiple myeloma

2019

Multiple myeloma (MM) is a hematologic malignancy characterized by high genomic instability. Here we provide evidence that hyper-activation of DNA ligase III (LIG3) is crucial for genomic instability and survival of MM cells. LIG3 mRNA expression in MM patients correlates with shorter survival and even increases with more advanced stage of disease. Knockdown of LIG3 impairs MM cells viability in vitro and in vivo, suggesting that neoplastic plasmacells are dependent on LIG3-driven repair. To investigate the mechanisms involved in LIG3 expression, we investigated the post-transcriptional regulation. We identified miR-22-3p as effective negative regulator of LIG3 in MM. Enforced expression of…

0301 basic medicineGenome instabilityCancer ResearchmiR-22 LIG3DNA repairDNA damageDNA repairApoptosisLIG3ArticleDNA Ligase ATP03 medical and health sciences0302 clinical medicinemicroRNABiomarkers TumorTumor Cells CulturedHumansPoly-ADP-Ribose Binding ProteinsCell ProliferationmiRNAchemistry.chemical_classificationRegulation of gene expressionGene knockdownDNA ligaseLeukemiamicroRNAChemistryHematologyPrognosisXenograft Model Antitumor AssaysGene Expression Regulation Neoplasticmultiple myelomaMicroRNAs030104 developmental biologyOncology030220 oncology & carcinogenesisCancer researchpharmacologyDNA DamageLeukemia
researchProduct

DNA Damage Signaling Instructs Polyploid Macrophage Fate in Granulomas.

2018

Granulomas are immune cell aggregates formed in response to persistent inflammatory stimuli. Granuloma macrophage subsets are diverse and carry varying copy numbers of their genomic information. The molecular programs that control the differentiation of such macrophage populations in response to a chronic stimulus, though critical for disease outcome, have not been defined. Here, we delineate a macrophage differentiation pathway by which a persistent Toll-like receptor (TLR) 2 signal instructs polyploid macrophage fate by inducing replication stress and activating the DNA damage response. Polyploid granuloma-resident macrophages formed via modified cell divisions and mitotic defects and not…

0301 basic medicineGenome instabilityDNA damageLipoproteinsCellMitosisInflammationAtaxia Telangiectasia Mutated ProteinsBiologymedicine.disease_causeGeneral Biochemistry Genetics and Molecular BiologyProto-Oncogene Proteins c-myc03 medical and health sciencesMicemedicineAnimalsHumansMacrophage Differentiation PathwayMitosisCell ProliferationInflammationGranulomaMacrophagesCell DifferentiationMycobacterium tuberculosisToll-Like Receptor 2Cell biologyMice Inbred C57BLTLR2030104 developmental biologymedicine.anatomical_structureImmunologymedicine.symptomCarcinogenesisDNA DamageCell
researchProduct

A dual role of caspase-8 in triggering and sensing proliferation-associated DNA damage, a key determinant of liver cancer development.

2017

Summary Concomitant hepatocyte apoptosis and regeneration is a hallmark of chronic liver diseases (CLDs) predisposing to hepatocellular carcinoma (HCC). Here, we mechanistically link caspase-8-dependent apoptosis to HCC development via proliferation- and replication-associated DNA damage. Proliferation-associated replication stress, DNA damage, and genetic instability are detectable in CLDs before any neoplastic changes occur. Accumulated levels of hepatocyte apoptosis determine and predict subsequent hepatocarcinogenesis. Proliferation-associated DNA damage is sensed by a complex comprising caspase-8, FADD, c-FLIP, and a kinase-dependent function of RIPK1. This platform requires a non-apop…

0301 basic medicineGenome instabilityMaleliver; Hepatocellular carcinoma; DNA damage response; replication stress; apoptosisCancer ResearchDNA RepairCarcinogenesisFas-Associated Death Domain ProteinApoptosisurologic and male genital diseasesDNA damage responseDna Damage Response ; Apoptosis ; Hepatocellular Carcinoma ; Liver ; Replication StressHistonesMice0302 clinical medicineRisk FactorsFADDPhosphorylationCellular SenescenceCaspase 8biologyLiver Neoplasmshepatocellular carcinomaLiver regeneration3. Good healthHistoneOncologyReceptors Tumor Necrosis Factor Type I030220 oncology & carcinogenesisReceptor-Interacting Protein Serine-Threonine KinasesFemalebiological phenomena cell phenomena and immunityCell agingCarcinoma HepatocellularDNA damageDNA repairreplication stressCaspase 8liverArticleGenomic Instability03 medical and health sciencesAnimalsHepatectomyHumansCrosses GeneticCell ProliferationJNK Mitogen-Activated Protein KinasesCell BiologyLiver Regeneration030104 developmental biologyImmunologyChronic Diseasebiology.proteinCancer researchHepatocytesMyeloid Cell Leukemia Sequence 1 ProteinDNA Damage
researchProduct

Inhibition of DNA damage response at telomeres improves the detrimental phenotypes of Hutchinson–Gilford Progeria Syndrome

2019

Hutchinson–Gilford progeria syndrome (HGPS) is a genetic disorder characterized by premature aging features. Cells from HGPS patients express progerin, a truncated form of Lamin A, which perturbs cellular homeostasis leading to nuclear shape alterations, genome instability, heterochromatin loss, telomere dysfunction and premature entry into cellular senescence. Recently, we reported that telomere dysfunction induces the transcription of telomeric non-coding RNAs (tncRNAs) which control the DNA damage response (DDR) at dysfunctional telomeres. Here we show that progerin-induced telomere dysfunction induces the transcription of tncRNAs. Their functional inhibition by sequence-specific telomer…

0301 basic medicineGenome instabilityRNA UntranslatedDNA RepairGeneral Physics and AstronomyCellular homeostasisAntisense oligonucleotide therapyMice0302 clinical medicineProgeriaHomeostasislcsh:ScienceCellular SenescenceSkinProgeriaMultidisciplinaryintegumentary systemQTelomereProgerinLamin Type A3. Good healthCell biologyTelomeresPhenotypePremature agingcongenital hereditary and neonatal diseases and abnormalitiesDNA repairScienceDouble-strand DNA breaksBiologySettore MED/08 - Anatomia PatologicaGeneral Biochemistry Genetics and Molecular BiologyArticleCell Line03 medical and health sciencesmedicineDNA damage Hutchinson-Gilford Progeria SyndromeAnimalsCell Proliferationnutritional and metabolic diseasesGeneral ChemistryOligonucleotides Antisensemedicine.diseaseTelomereDisease Models Animal030104 developmental biologyMutationlcsh:Q030217 neurology & neurosurgeryLaminDNA DamageNature Communications
researchProduct

Targeting aging with functional food: Pasta with opuntia single-arm pilot study

2018

Interventions to extend life span represent the new perspective in aging investigation. Healthy dietary habits are important modifiable factors that can favor a healthy aging phenotype. Many studies have demonstrated benefits for metabolic syndrome and type 2 diabetes mellitus resulting from the traditional Mediterranean foods. Opuntia Ficus Indica (OFI), widespread in the Mediterranean basin, belongs to the Cactaceae family. It is known for its antioxidant and anti-inflammatory properties. Moreover, products containing extracts from OFI fruits or cladodes have been used to control obesity and other metabolic parameters, such as glycemia and lipid profile. The aim of this study was to analy…

0301 basic medicineGerontologyAdultMaleAgingMediterranean dietLongevityPsychological interventionAnti-Inflammatory AgentsPilot Projects030204 cardiovascular system & hematologyBiologyAntioxidantsOpuntia Ficus Indica03 medical and health sciencesYoung Adult0302 clinical medicineFunctional foodFunctional FoodMediterranean dietDiabetes MellitusHumansLongitudinal StudiesObesityHealthy agingAgedCell ProliferationInflammationMetabolic Syndromeage-related diseaseoxidative streLife spanTraditional medicinePlant ExtractsPerspective (graphical)food and beveragesOpuntiaMiddle AgedHealthy VolunteersOxidative Stress030104 developmental biologyPhenotypenutritionDiabetes Mellitus Type 2Cardiovascular DiseasesDietary SupplementsFemaleGeriatrics and Gerontology
researchProduct