Search results for "PROLIFERATION"

showing 10 items of 1193 documents

GDF11 exhibits tumor suppressive properties in hepatocellular carcinoma cells by restricting clonal expansion and invasion.

2019

Growth differentiation factor 11 (GDF11) has been characterized as a key regulator of differentiation in cells that retain stemness features, despite some controversies in age-related studies. GDF11 has been poorly investigated in cancer, particularly in those with stemness capacity, such as hepatocellular carcinoma (HCC), one of the most aggressive cancers worldwide. Here, we focused on investigating the effects of GDF11 in liver cancer cells. GDF11 treatment significantly reduced proliferation, colony and spheroid formation in HCC cell lines. Consistently, down-regulation of CDK6, cyclin D1, cyclin A, and concomitant upregulation of p27 was observed after 24 h of treatment. Interestingly,…

0301 basic medicine[SDV]Life Sciences [q-bio]Cyclin ACellChick EmbryoChorioallantoic Membrane0302 clinical medicineCell MovementCyclin D1HCCbiologyNeovascularization PathologicCell DifferentiationHep G2 CellsCell cycleCadherinsHuh7 cells3. Good health[SDV] Life Sciences [q-bio]Gene Expression Regulation NeoplasticGrowth Differentiation Factorsmedicine.anatomical_structure030220 oncology & carcinogenesisBone Morphogenetic ProteinsMolecular MedicineLiver cancerCyclin-Dependent Kinase Inhibitor p27Signal Transduction[SDV.CAN]Life Sciences [q-bio]/CancerCyclin ACell cycleHep3B cells03 medical and health sciencesCyclin D1Downregulation and upregulation[SDV.CAN] Life Sciences [q-bio]/CancerAntigens CDCell Line TumorOccludinSpheroids CellularmedicineAnimalsHumansViability assayMolecular BiologyCell Proliferation[SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and GastroenterologyCyclin-Dependent Kinase 6[SDV.MHEP.HEG] Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterology030104 developmental biologyCell cultureGDF11biology.proteinCancer researchCyclin-dependent kinase 6Snail Family Transcription FactorsBiochimica et biophysica acta. Molecular basis of disease
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Impaired Kupffer Cell Self-Renewal Alters the Liver Response to Lipid Overload during Non-alcoholic Steatohepatitis

2020

International audience; Kupffer cells (KCs) are liver-resident macrophages that self-renew by proliferation in the adult independently from monocytes. However, how they are maintained during non-alcoholic steatohepatitis (NASH) remains ill defined. We found that a fraction of KCs derived from Ly-6C+ monocytes during NASH, underlying impaired KC self-renewal. Monocyte-derived KCs (MoKCs) gradually seeded the KC pool as disease progressed in a response to embryo-derived KC (EmKC) death. Those MoKCs were partly immature and exhibited a pro-inflammatory status compared to EmKCs. Yet, they engrafted the KC pool for the long term as they remained following disease regression while acquiring matur…

0301 basic medicine[SDV]Life Sciences [q-bio]OntogenyMESH: Cell Self RenewalSelf renewalMESH: MonocytesMESH: Mice KnockoutMice0302 clinical medicineNon-alcoholic Fatty Liver DiseaseImmunology and AllergyKupffer cellsMESH: AnimalsCell Self RenewalMESH: Lipid MetabolismMice KnockoutKupffer cellLipidsResearch Highlightmacrophages[SDV] Life Sciences [q-bio]Infectious Diseasesmedicine.anatomical_structureLiver030220 oncology & carcinogenesismonocytesmedicine.medical_specialtynon-alcoholic steatohepatitis (NASH)ImmunologyBiology03 medical and health sciencesMESH: Mice Inbred C57BLMESH: Cell ProliferationInternal medicinemedicineAnimalsLiver damageMESH: MiceCell ProliferationMESH: Non-alcoholic Fatty Liver DiseaseTriglyceride storageNon alcoholicLipid Metabolismmedicine.diseaseMESH: Lipidseye diseasesMice Inbred C57BLMESH: Kupffer Cells030104 developmental biologyEndocrinologySteatohepatitisHomeostasisMESH: LiverImmunity
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The histone deacetylase inhibitor SAHA induces HSP60 nitration and its extracellular release by exosomal vesicles in human lung-derived carcinoma cel…

2015

// Claudia Campanella 1, 2, * , Antonella D'Anneo 3, * , Antonella Marino Gammazza 1, 2, * , Celeste Caruso Bavisotto 1, 2 , Rosario Barone 1, 2 , Sonia Emanuele 4 , Filippa Lo Cascio 1 , Emanuele Mocciaro 1 , Stefano Fais 5 , Everly Conway De Macario 6 , Alberto J.L. Macario 2, 6 , Francesco Cappello 1, 2 , Marianna Lauricella 4 1 Department of Experimental Biomedicine and Clinical Neurosciences, Section of Human Anatomy “Emerico Luna”, University of Palermo, Palermo, Italy 2 Euro-Mediterranean Institute of Science and Technology, Palermo, Italy 3 Department of Biological, Chemical and Pharmaceutical Sciences and Technologies, Laboratory of Biochemistry, University of Palermo, Palermo, Ita…

0301 basic medicineanimal structuresLung Neoplasmsmedicine.drug_classCell SurvivalNitrosationExosomes; Histone deacetylase inhibitor; HSP60; Oxidative stress; SAHAchemical and pharmacologic phenomenaAntineoplastic AgentsApoptosisexosomesBiologyHydroxamic Acidscomplex mixturesMitochondrial Proteins03 medical and health sciencesCell Line TumorSettore BIO/10 - BiochimicamedicineHumansoxidative stressSecretionViability assayCell ProliferationVorinostatHistone deacetylase inhibitorCell growthSettore BIO/16 - Anatomia UmanaHistone deacetylase inhibitorfungiSAHAChaperonin 60MicrovesiclesHistone Deacetylase InhibitorsExosome030104 developmental biologyOncologyApoptosisImmunologyCancer researchOxidative streHSP60Histone deacetylaseProtein Processing Post-TranslationalHSP60Research Paper
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Effects of Pimozide Derivatives on pSTAT5 in K562 Cells

2017

STAT5 is a transcription factor, a member of the STAT family of signaling proteins. STAT5 is involved in many types of cancer, including chronic myelogenous leukemia (CML), in which this protein is found constitutively activated as a consequence of BCR-ABL expression. The neuroleptic drug pimozide was recently reported to act as an inhibitor of STAT5 phosphorylation and is capable of inducing apoptosis in CML cells in vitro. Our research group has synthesized simple derivatives of pimozide with cytotoxic activity and that are able to decrease the levels of phosphorylated STAT5. In this work we continued the search for novel STAT5 inhibitors, synthesizing compounds in which the benzoimidazol…

0301 basic medicineantiproliferationApoptosisPharmacologyBiochemistryAntineoplastic Agent0302 clinical medicinePimozidehemic and lymphatic diseasesDrug DiscoverySTAT5 Transcription FactorCytotoxic T cellPhosphorylationGeneral Pharmacology Toxicology and PharmaceuticsBCR-ABL-expressing leukemia; STAT5 inhibitors; antiproliferation; apoptosis; pimozideSTAT5Molecular StructurebiologyPimozidefood and beverages030220 oncology & carcinogenesisMolecular MedicinePhosphorylationHumanmedicine.drugAntineoplastic AgentsNOStructure-Activity Relationship03 medical and health sciencesK562 CellmedicineHumansTranscription factorCell ProliferationPharmacologyDose-Response Relationship DrugCell growthSTAT5 inhibitorsOrganic ChemistryApoptosiSTAT5 inhibitormedicine.disease030104 developmental biologyPharmacology Toxicology and Pharmaceutics (all)biology.proteinCancer researchBCR-ABL-expressing leukemiaDrug Screening Assays AntitumorK562 CellsK562 cellsChronic myelogenous leukemiaChemMedChem
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Artesunate Impairs Growth in Cisplatin-Resistant Bladder Cancer Cells by Cell Cycle Arrest, Apoptosis and Autophagy Induction

2020

Cisplatin, which induces DNA damage, is standard chemotherapy for advanced bladder cancer (BCa). However, efficacy is limited due to resistance development. Since artesunate (ART), a derivative of artemisinin originating from Traditional Chinese Medicine, has been shown to exhibit anti-tumor activity, and to inhibit DNA damage repair, the impact of artesunate on cisplatin-resistant BCa was evaluated. Cisplatin-sensitive (parental) and cisplatin-resistant BCa cells, RT4, RT112, T24, and TCCSup, were treated with ART (1&ndash

0301 basic medicineautophagyRMCell cycle checkpointDNA RepairDNA damageArtesunateCell Cycle ProteinsArticlegrowth inhibition03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCell Line TumormedicineHumansddc:610Medicine Chinese Traditionalskin and connective tissue diseaseslcsh:QH301-705.5Cell ProliferationCisplatinartesunate (ART)Cell growthAutophagyapoptosisGeneral MedicineCell cycleG1 Phase Cell Cycle Checkpoints030104 developmental biologychemistrylcsh:Biology (General)Urinary Bladder NeoplasmsApoptosisDrug Resistance Neoplasm030220 oncology & carcinogenesisCancer researchbladder cancer (BCa)Growth inhibitioncisplatin resistanceMicrotubule-Associated Proteinsmedicine.drug
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Effect of Manganese Chloride and of Cotreatment with Cadmium Chloride on the In Vitro Proliferative, Motile, and Invasive Behavior of MDA-MB231 Breas…

2019

We examined the dose&ndash

0301 basic medicinecadmiumproliferationPharmaceutical ScienceBreast NeoplasmsCadmium chloridemedicine.disease_causeArticleAnalytical ChemistryMetastasislcsh:QD241-44103 medical and health scienceschemistry.chemical_compound0302 clinical medicineBreast cancerCadmium ChlorideChlorideslcsh:Organic chemistryCell Movementbreast cancer cellCell Line TumorDrug DiscoverymedicineHumansSettore BIO/06 - Anatomia Comparata E CitologiaPhysical and Theoretical ChemistrychemotaxisCell ProliferationCell growthOrganic Chemistrymedicine.diseasechemoinvasionIn vitroEpithelium030104 developmental biologymedicine.anatomical_structureManganese CompoundschemistryChemistry (miscellaneous)030220 oncology & carcinogenesisCancer cellCancer researchmanganeseMolecular MedicineFemalechemotaxiCarcinogenesisbreast cancer cellsMolecules
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Loss of MCL1 function sensitizes the MDA-MB-231 breast cancer cells to rh-TRAIL by increasing DR4 levels.

2019

Triple-negative breast cancer (TNBC) is a form of BC characterized by high aggressiveness and therapy resistance probably determined by cancer stem cells. MCL1 is an antiapoptotic Bcl-2 family member that could limit the efficacy of anticancer agents as recombinant human tumor necrosis factor related apoptosis-inducing ligand (rh-TRAIL). Here, we investigated MCL1 expression in TNBC tissues and cells. We found MCL1 differentially expressed (upregulated or downregulated) in TNBC tissues. Furthermore, in comparison to the human mammary epithelial cells, we found that MDA-MB-231 cells show similar messenger RNA levels but higher MCL1 protein levels, whereas it resulted downregulated in MDA-MB-…

0301 basic medicinecancer stem cellIndolesPhysiologyCell SurvivalClinical BiochemistryCellPopulationApoptosisTNF-Related Apoptosis-Inducing Ligand03 medical and health sciences0302 clinical medicineCancer stem cellSettore BIO/10 - BiochimicaCell Line Tumormedicinerh-TRAILBiomarkers TumorGene silencingHumansViability assayGene SilencingeducationCell ShapeCell ProliferationMembrane Potential Mitochondrialeducation.field_of_studySulfonamidesChemistryCell growthCell CycleCell BiologyCell cycleRecombinant ProteinsGene Expression Regulation NeoplasticReceptors TNF-Related Apoptosis-Inducing Ligand030104 developmental biologymedicine.anatomical_structureMCL1ApoptosisDR4 receptor030220 oncology & carcinogenesisCancer researchtriple-negative breast cancerMyeloid Cell Leukemia Sequence 1 ProteinJournal of cellular physiology
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MiR-24 induces chemotherapy resistance and hypoxic advantage in breast cancer

2017

// Giuseppina Roscigno 1, 2, * , Ilaria Puoti 1, 2, * , Immacolata Giordano 1 , Elvira Donnarumma 3 , Valentina Russo 1 , Alessandra Affinito 1 , Assunta Adamo 1 , Cristina Quintavalle 1, 2 , Matilde Todaro 4 , Maria dM Vivanco 5 , Gerolama Condorelli 1, 2 1 Department of Molecular Medicine and Medical Biotechnology, “Federico II” University of Naples, Naples, Italy 2 IEOS, CNR, Naples, Italy 3 IRCCS-SDN, Naples, Italy 4 Department of Pathobiology and Medical Biotechnology, University of Palermo, Palermo, Italy 5 CIC bioGUNE, Centre for Cooperative Research in Biosciences, Derio, Spain * These authors have contributed equally to the paper as first authors Correspondence to: Gerolama Condore…

0301 basic medicinecancer stem cellsApoptosisStem cell markermedicine.disease_causemicroRNAs Breast cancer Cancer stem cells BimL FIH1Mixed Function OxygenasesAntineoplastic Agent0302 clinical medicineCell MovementTumor Cells CulturedCell Self RenewalMixed Function OxygenaseBimLmicroRNACell HypoxiamicroRNAsGene Expression Regulation NeoplasticOncology030220 oncology & carcinogenesisNeoplastic Stem CellsFemaleBreast NeoplasmAdult stem cellHumanResearch PaperFIH1BimL; FIH1; breast cancer; cancer stem cells; microRNAsAntineoplastic AgentsBreast Neoplasms03 medical and health sciencesBreast cancerbreast cancerDownregulation and upregulationCancer stem cellmicroRNAmedicineBiomarkers TumorHumansCell Proliferationbusiness.industryCancer stem cellApoptosiRepressor Proteinmedicine.diseaseHypoxia-Inducible Factor 1 alpha SubunitMolecular medicineRepressor Proteins030104 developmental biologyDrug Resistance NeoplasmImmunologyCancer researchNeoplastic Stem CellCisplatinCarcinogenesisbusiness
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Bisphenolic compounds alter gene expression in MCF-7 cells through interaction with estrogen receptor α

2020

Plasticizers released from microplastic are increasingly viewed with concern. While adverse health effects induced by bisphenol A and its analogues on marine animals are well documented in the literature, the endocrine potential of bisphenolic compounds on human health remains elusive. We applied next generation sequencing (NGS) with the estrogen receptor α (ERα) positive human breast cancer cell line MCF-7 treated with 17-β-estradiol (E2), bisphenol A (BPA), bisphenol B (BPB), bisphenol Z (BPZ) and tetramethyl bisphenol A (4MeBPA). We used molecular docking, microscale thermophoresis, ERα activation assay, and cell cycle experiments on MCF-7 and ERα overexpressing HEK293 cells to verify th…

0301 basic medicineendocrine systemBisphenolDown-RegulationGene ExpressionEstrogen receptorBreast NeoplasmsEndocrine DisruptorsToxicologyCell Line03 medical and health sciences0302 clinical medicinePhenolsPlasticizersBCAS3Cell Line TumorHumansBenzhydryl CompoundsCell ProliferationInsulin-like growth factor 1 receptorPharmacologyEstradiolChemistryCell growthEstrogen Receptor alphaEstrogensCell cycleUp-RegulationHEK293 Cells030104 developmental biologyPRKCDMCF-7030220 oncology & carcinogenesisMCF-7 CellsCancer researchFemalehormones hormone substitutes and hormone antagonistsSignal TransductionToxicology and Applied Pharmacology
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Extracellular Superoxide Dismutase Expression in Papillary Thyroid Cancer Mesenchymal Stem/Stromal Cells Modulates Cancer Cell Growth and Migration

2017

AbstractTumor stroma-secreted growth factors, cytokines, and reactive oxygen species (ROS) influence tumor development from early stages to the metastasis phase. Previous studies have demonstrated downregulation of ROS-producing extracellular superoxide dismutase (SOD3) in thyroid cancer cell lines although according to recent data, the expression of SOD3 at physiological levels stimulates normal and cancer cell proliferation. Therefore, to analyze the expression of SOD3 in tumor stroma, we characterized stromal cells from the thyroid. We report mutually exclusive desmoplasia and inflammation in papillary and follicular thyroid cancers and the presence of multipotent mesenchymal stem/stroma…

0301 basic medicineendocrine systemPathologymedicine.medical_specialtyStromal cellendocrine system diseasesThyroid GlandBiologyArticleMetastasisPapillary thyroid cancer03 medical and health sciences0302 clinical medicineCell MovementExtracellular ;Thyroid ;Cancer ;Cell .Adenocarcinoma FollicularParacrine CommunicationBiomarkers TumormedicineHumansThyroid NeoplasmsThyroid cancerCell ProliferationMultidisciplinarySuperoxide DismutaseMesenchymal stem cellThyroidEpithelial CellsMesenchymal Stem Cellsmedicine.diseaseFibrosisCarcinoma PapillaryDesmoplasiaGene Expression Regulation NeoplasticPhenotype030104 developmental biologymedicine.anatomical_structureThyroid Cancer Papillary030220 oncology & carcinogenesisCancer cellmedicine.symptomExtracellular SpaceScientific Reports
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