Search results for " Cell proliferation."

showing 10 items of 65 documents

Improvement of osteogenic differentiation of human mesenchymal stem cells on composite poly l-lactic acid/nano-hydroxyapatite scaffolds for bone defe…

2020

Tissue engineering offers new approaches to repair bone defects, which cannot be repaired physiologically, developing scaffolds that mimic bone tissue architecture. Furthermore, biomechanical stimulation induced by bioreactor, provides biomechanical cues that regulate a wide range of cellular events especially required for cellular differentiation and function. The improvement of human mesenchymal stem cells (hMSCs) colonization in poly-L-lactic-acid (PLLA)/nano- hydroxyapatite (nHA) composite scaffold was evaluated in terms of cell proliferation (dsDNA content), bone differen- tiation (gene expression and protein synthesis) and ultrastructural analysis by comparing static (s3D) and dynamic…

0106 biological sciences0301 basic medicine3D cultureScaffoldCellular differentiationBioreactorBioengineeringBone tissue01 natural sciencesApplied Microbiology and BiotechnologyBone and BonesCell Line03 medical and health sciencesBioreactorsTissue engineeringPolylactic Acid-Polyglycolic Acid CopolymerPoly-L-lactic-acid/nano-hydroxyapatiteOsteogenesis010608 biotechnologyOsteogenic differentiation w/o growth factorsmedicineHumansBone regenerationCell ProliferationComposite scaffoldSettore ING-IND/24 - Principi Di Ingegneria ChimicaTissue EngineeringTissue ScaffoldsChemistryMesenchymal stem cell3D culture; Bioreactor; Composite scaffold; Osteogenic differentiation w/o growth factors; Poly-L-lactic-acid/nano-hydroxyapatite; Bioreactors; Bone and Bones; Cell Differentiation; Cell Line; Cell Proliferation; Durapatite; Humans; Mesenchymal Stem Cells; Osteogenesis; Polylactic Acid-Polyglycolic Acid Copolymer; Tissue Engineering; Tissue ScaffoldsSettore ING-IND/34 - Bioingegneria IndustrialeCell DifferentiationMesenchymal Stem CellsCell biologyRUNX2030104 developmental biologymedicine.anatomical_structureDurapatiteCell cultureBiotechnologyJournal of bioscience and bioengineering
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Retinoic Acid affects Lung Adenocarcinoma growth by inducing differentiation via GATA6 activation and EGFR and Wnt inhibition

2016

AbstractA fundamental task in cancer research aims at the identification of new pharmacological therapies that can affect tumor growth. Differentiation therapy might exploit this function not only for hematological diseases, such as acute promyelocytic leukemia (APML) but also for epithelial tumors, including lung cancer. Here we show that Retinoic Acid (RA) arrests in vitro and in vivo the growth of Tyrosine Kinase Inhibitors (TKI) resistant Non Small Cell Lung Cancer (NSCLC). In particular, we found that RA induces G0/G1 cell cycle arrest in TKI resistant NSCLC cells and activates terminal differentiation programs by modulating the expression of GATA6, a key transcription factor involved …

0301 basic medicineAcute promyelocytic leukemiaScienceEGFRRetinoic acidMice NudeTretinoinBiologyArticle03 medical and health scienceschemistry.chemical_compoundDifferentiation therapySettore BIO/13 - Biologia ApplicataCarcinoma Non-Small-Cell LungCell Line TumorGATA6 Transcription FactormedicineRetinoic acidAnimalsHumansLung cancerProtein Kinase InhibitorsWnt Signaling PathwayTranscription factorCell ProliferationMultidisciplinaryQRWnt signaling pathwayCell Differentiationmedicine.diseaseG1 Phase Cell Cycle CheckpointsXenograft Model Antitumor Assaysrespiratory tract diseasesErbB Receptorslung cancerAnimals; Carcinoma Non-Small-Cell Lung; Cell Differentiation; Cell Line Tumor; Cell Proliferation; Drug Resistance Neoplasm; ErbB Receptors; G1 Phase Cell Cycle Checkpoints; GATA6 Transcription Factor; Humans; Mice Nude; Protein Kinase Inhibitors; Signal Transduction; Tretinoin; Wnt Signaling Pathway; Xenograft Model Antitumor Assays030104 developmental biologychemistryDrug Resistance NeoplasmImmunologyCancer researchMedicineAdenocarcinomaEngineering sciences. TechnologyTyrosine kinaseSignal Transduction
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Novel iodoacetamido benzoheterocyclic derivatives with potent antileukemic activity are inhibitors of STAT5 phosphorylation

2016

Signal Transducer and Activator of Transcription 5 (STAT5) protein, a component of the STAT family of signaling proteins, is considered to be an attractive therapeutic target because of its involvement in the progression of acute myeloid leukemia. In an effort to discover potent molecules able to inhibit the phosphorylation-activation of STAT5, twenty-two compounds were synthesized and evaluated on the basis of our knowledge of the activity of 2-(3’,4’,5’-trimethoxybenzoyl)-3-iodoacetamido-6-methoxy benzo[b]furan derivative 1 as a potent STAT5 inhibitor. Most of these molecules, structurally related to compound 1, were characterized by the presence of a common 3’,4’,5’-trimethoxybenzoyl moi…

0301 basic medicineApoptosisAntineoplastic Agentchemistry.chemical_compoundBenzophenone0302 clinical medicinehemic and lymphatic diseasesFuranDrug DiscoverySTAT5 Transcription FactorTumor Cells CulturedThiopheneMoietyPhosphorylationSTAT5Molecular StructurebiologyChemistryBiological activityGeneral MedicineApoptosis; BCR/ABL expressing leukemia; In vitro antiproliferative activity; STAT5 inhibitors; Structure-activity relationship; Drug Discovery3003 Pharmaceutical Science; Organic Chemistry; PharmacologyLeukemia Myeloid Acute030220 oncology & carcinogenesisBCR/ABL expressing leukemiaApoptosis; BCR/ABL expressing leukemia; In vitro antiproliferative activity; STAT5 inhibitors; Structure-activity relationship; Antineoplastic Agents; Apoptosis; Benzofurans; Benzophenones; Cell Proliferation; Dose-Response Relationship Drug; Drug Screening Assays Antitumor; Humans; K562 Cells; Leukemia Myeloid Acute; Molecular Structure; Phosphorylation; STAT5 Transcription Factor; Structure-Activity Relationship; Tumor Cells Cultured; Drug Discovery3003 Pharmaceutical Science; Organic Chemistry; PharmacologyHumanStereochemistryAntineoplastic AgentsArticleNOBenzophenones03 medical and health sciencesK562 CellHumansStructure–activity relationshipBenzofuransCell ProliferationPharmacologyIndole testDose-Response Relationship DrugIn vitro antiproliferative activitySTAT5 inhibitorsDrug Discovery3003 Pharmaceutical ScienceOrganic ChemistryApoptosiSTAT5 inhibitorStructure-activity relationshipIn vitro030104 developmental biologybiology.proteinBenzofuranDrug Screening Assays AntitumorK562 Cells
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The phospholipase DDHD1 as a new target in colorectal cancer therapy

2018

Background Our previous study demonstrates that Citrus-limon derived nanovesicles are able to decrease colon cancer cell viability, and that this effect is associated with the downregulation of the intracellular phospholipase DDHD domain-containing protein 1 (DDHD1). While few studies are currently available on the contribution of DDHD1 in neurological disorders, there is no information on its role in cancer. This study investigates the role of DDHD1 in colon cancer. Methods DDHD1 siRNAs and an overexpression vector were transfected into colorectal cancer and normal cells to downregulate or upregulate DDHD1 expression. In vitro and in vivo assays were performed to investigate the functional…

0301 basic medicineCancer ResearchColorectal cancerApoptosisMiceSettore BIO/13 - Biologia ApplicataGene Regulatory NetworksMolecular Targeted TherapyCitrus-limon nanovesicleTransfectionlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens3. Good healthCitrus-limon nanovesicles; Colorectal cancer; Phospholipase DDHD1; Oncology; Cancer ResearchOncologyPhospholipasesCitrus-limon nanovesicles; Colorectal cancer; Phospholipase DDHD1; Animals; Antineoplastic Agents; Apoptosis; Cell Line Tumor; Cell Proliferation; Colorectal Neoplasms; Computational Biology; Disease Models Animal; Female; Gene Expression Profiling; Gene Ontology; Gene Regulatory Networks; Gene Silencing; Humans; MAP Kinase Signaling System; Mice; Phospholipases; Signal Transduction; Xenograft Model Antitumor Assays; Biomarkers Tumor; Molecular Targeted TherapyFemaleColorectal NeoplasmsSignal TransductionMAP Kinase Signaling SystemAntineoplastic Agentslcsh:RC254-282Citrus-limon nanovesicles03 medical and health sciencesDownregulation and upregulationIn vivoCell Line TumorBiomarkers TumormedicineAnimalsHumansGene silencingGene SilencingPhospholipase DDHD1Cell Proliferationbusiness.industryCell growthGene Expression ProfilingResearchComputational BiologyCancermedicine.diseaseXenograft Model Antitumor AssaysColorectal cancerDisease Models AnimalGene Ontology030104 developmental biologyApoptosisCancer researchbusiness
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A receptor-antibody hybrid hampering MET-driven metastatic spread

2021

AbstractBackgroundThe receptor encoded by the MET oncogene and its ligand Hepatocyte Growth Factor (HGF) are at the core of the invasive-metastatic behavior. In a number of instances genetic alterations result in ligand-independent onset of malignancy (METaddiction). More frequently, ligand stimulation of wild-type MET contributes to progression toward metastasis (METexpedience). Thus, while MET inhibitors alone are effective in the first case, combination therapy with ligand inhibitors is required in the second condition.MethodsIn this paper, we generated hybrid molecules gathering HGF and MET inhibitory properties. This has been achieved by ‘head-to-tail’ or ‘tail-to-head’ fusion of a sin…

0301 basic medicineCancer ResearchImmunoconjugatesmedicine.medical_treatmentMice SCIDEpitopeFusion proteins; HGF; MET; Metastasis; Targeted therapy; A549 Cells; Animals; Binding Sites Antibody; Cell Line Tumor; Cell Proliferation; Female; Hepatocyte Growth Factor; Humans; Immunoconjugates; Immunoglobulin Fab Fragments; Mice; Mice SCID; Neoplasm Metastasis; Neoplasms; Proto-Oncogene Proteins c-met; Rats; Rats Sprague-Dawley; Recombinant Proteins; Xenograft Model Antitumor AssaysMetastasisTargeted therapyMetastasisRats Sprague-DawleyTargeted therapyMice0302 clinical medicineNeoplasmsHGFNeoplasm MetastasisReceptorTumorHepatocyte Growth FactorChemistryProto-Oncogene Proteins c-metlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensRecombinant ProteinsOncology030220 oncology & carcinogenesisMETFemaleHepatocyte growth factormedicine.drugSCIDlcsh:RC254-282Cell LineImmunoglobulin Fab Fragments03 medical and health sciencesCell Line TumorPancreatic cancermedicineAnimalsHumansAntibodyCell ProliferationBinding SitesResearchmedicine.diseaseXenograft Model Antitumor AssaysFusion proteinRatsFusion proteins030104 developmental biologyA549 CellsCancer cellCancer researchBinding Sites AntibodySprague-DawleyJournal of Experimental & Clinical Cancer Research
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Nicotinamide Phosphoribosyltransferase Acts as a Metabolic Gate for Mobilization of Myeloid-Derived Suppressor Cells

2019

Abstract Cancer induces alteration of hematopoiesis to fuel disease progression. We report that in tumor-bearing mice the macrophage colony-stimulating factor elevates the myeloid cell levels of nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in the NAD salvage pathway, which acts as negative regulator of the CXCR4 retention axis of hematopoietic cells in the bone marrow. NAMPT inhibits CXCR4 through a NAD/Sirtuin 1–mediated inactivation of HIF1α-driven CXCR4 gene transcription, leading to mobilization of immature myeloid-derived suppressor cells (MDSC) and enhancing their production of suppressive nitric oxide. Pharmacologic inhibition or myeloid-specific ablation …

0301 basic medicineCancer ResearchMyeloidmedicine.medical_treatmentNudeNicotinamide phosphoribosyltransferaseApoptosisColorectal NeoplasmInbred C57BLMicechemistry.chemical_compound0302 clinical medicineTumor Cells CulturedHematopoiesiNicotinamide PhosphoribosyltransferaseInbred BALB CMice Inbred BALB CCulturedbiologySarcomaTumor CellsHaematopoiesismedicine.anatomical_structureOncology030220 oncology & carcinogenesisSirtuinFemaleSarcoma ExperimentalColorectal NeoplasmsAnimals; Apoptosis; Cell Proliferation; Colorectal Neoplasms; Female; Hematopoiesis; Humans; Mammary Neoplasms Experimental; Mice; Mice Inbred BALB C; Mice Inbred C57BL; Mice Nude; Myeloid-Derived Suppressor Cells; NAD; Nicotinamide Phosphoribosyltransferase; Sarcoma Experimental; Signal Transduction; Tumor Cells Cultured; Xenograft Model Antitumor AssaysHumanSignal TransductionMice NudeExperimental03 medical and health sciencesmedicineMyeloid-Derived Suppressor CellAnimalsHumansCell ProliferationAnimalMyeloid-Derived Suppressor CellsMammary NeoplasmsApoptosiMammary Neoplasms ExperimentalImmunotherapyNADXenograft Model Antitumor AssaysHematopoiesisMice Inbred C57BL030104 developmental biologychemistrybiology.proteinCancer researchMyeloid-derived Suppressor CellNAD+ kinaseBone marrowCancer Research
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Persistent immune stimulation exacerbates genetically driven myeloproliferative disorders via stromal remodeling

2017

Abstract Systemic immune stimulation has been associated with increased risk of myeloid malignancies, but the pathogenic link is unknown. We demonstrate in animal models that experimental systemic immune activation alters the bone marrow stromal microenvironment, disarranging extracellular matrix (ECM) microarchitecture, with downregulation of secreted protein acidic and rich in cysteine (SPARC) and collagen-I and induction of complement activation. These changes were accompanied by a decrease in Treg frequency and by an increase in activated effector T cells. Under these conditions, hematopoietic precursors harboring nucleophosmin-1 (NPM1) mutation generated myeloid cells unfit for normal …

0301 basic medicineCancer ResearchStromal cellMyeloidMice TransgenicVascular RemodelingBiologyInbred C57BLTransgenicMice03 medical and health sciencesMyelogenousMyeloproliferative DisordersmedicineAnimalsHumansMyeloproliferative DisorderAnimals; Cell Proliferation; Humans; Mice; Mice Inbred C57BL; Mice Inbred CBA; Mice Transgenic; Myeloproliferative Disorders; Stromal Cells; Vascular Remodeling; Oncology; Cancer ResearchCell ProliferationMyeloproliferative DisordersAnimalStromal CellInbred CBANeutrophil extracellular trapsmedicine.diseaseMice Inbred C57BLHaematopoiesisLeukemia030104 developmental biologymedicine.anatomical_structureOncologyImmunologyMice Inbred CBABone marrowStromal CellsNucleophosminHuman
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Peroxisome proliferator-activated receptor alpha deficiency impairs regulatory T cell functions: Possible application in the inhibition of melanoma t…

2016

International audience; Regulatory T (Treg) cells are important to induce and maintain immunological self-tolerance. Although the progress accomplished in understanding the functional mechanism of Treg cells, intracellular molecules that control the mechanisms of their suppressive capacity are still on investigation. The present study showed that peroxisome proliferator-activated receptor-alpha deficiency impaired the suppressive activity of Treg cells on CD4(+)CD25(-) and CD8(+) T cell proliferation. In Treg cells, PPARα gene deletion also induced a decrease of migratory abilities, and downregulated the expression of chemokine receptors (CCR-4, CCR-8 and CXCR-4) and p27(KIP1) mRNA. Treg ce…

0301 basic medicineMaleAdoptive cell transferMESH: Tumor BurdenB16 melanoma tumorMelanoma ExperimentalMESH: T-Lymphocyte SubsetsCD4(+)CD25(+) regulatory T cellsBiochemistryMESH: Mice KnockoutImmunotherapy AdoptiveT-Lymphocytes RegulatoryPPARαMESH : T-Lymphocytes RegulatoryCell MovementT-Lymphocyte SubsetsMESH: Reverse Transcriptase Polymerase Chain ReactionMESH : Cell ProliferationMESH : Cell MovementMESH: AnimalsIL-2 receptorMESH: PPAR alphaMESH: Cell MovementCells CulturedMice KnockoutMESH : Melanoma ExperimentalbiologyMESH : Tumor BurdenReverse Transcriptase Polymerase Chain ReactionMESH : Reverse Transcriptase Polymerase Chain ReactionFOXP3hemic and immune systemsGeneral MedicineMESH: Gene Expression Regulation Neoplastic3. Good healthTumor BurdenMESH: Melanoma ExperimentalDNA-Binding ProteinsGene Expression Regulation Neoplasticmedicine.anatomical_structureMESH: Immunotherapy AdoptiveReceptors ChemokineMESH : DNA-Binding ProteinsMESH: Cells Culturedmedicine.medical_specialtyMESH : Receptors ChemokineMESH: Cell Line TumorRegulatory T cellMESH : Gene Expression Regulation NeoplasticT cellMESH : MaleMESH : PPAR alphachemical and pharmacologic phenomenaMESH : Mice Inbred C57BLMESH : Clonal Anergy03 medical and health sciencesMESH: Mice Inbred C57BLInternal medicineMESH: Cell ProliferationCell Line TumorMESH : Cells CulturedmedicineAnimals[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyPPAR alpha[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyCell ProliferationClonal AnergyPerforinMESH : Cell Line TumorMESH: T-Lymphocytes RegulatoryMolecular biologyMESH: MaleMESH : T-Lymphocyte SubsetsGranzyme BMice Inbred C57BL030104 developmental biologyEndocrinologyPerforinMESH: Clonal Anergybiology.proteinMESH : Mice KnockoutMESH : AnimalsMESH: Receptors ChemokineCD8MESH: DNA-Binding ProteinsMESH : Immunotherapy Adoptive
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Interleukin 3- receptor targeted exosomes inhibit in vitro and in vivo chronic myelogenous Leukemia cell growth

2017

Despite Imatinib (IM), a selective inhibitor of Bcr-Abl, having led to improved prognosis in Chronic Myeloid Leukemia (CML) patients, acquired resistance and long-term adverse effects is still being encountered. There is, therefore, urgent need to develop alternative strategies to overcome drug resistance. According to the molecules expressed on their surface, exosomes can target specific cells. Exosomes can also be loaded with a variety of molecules, thereby acting as a vehicle for the delivery of therapeutic agents. In this study, we engineered HEK293T cells to express the exosomal protein Lamp2b, fused to a fragment of Interleukin 3 (IL3). The IL3 receptor (IL3-R) is overexpressed in CML…

0301 basic medicineMedicine (miscellaneous)PharmacologyEngineered exosomeExosomesInterleukin 3Antineoplastic AgentMiceHEK293 Cellhemic and lymphatic diseasesDrug CarrierPharmacology Toxicology and Pharmaceutics (miscellaneous)Drug CarriersChronic myeloid leukemiaMyeloid leukemiaChronic myeloid leukemia; Drug delivery; Drug resistance; Engineered exosomes; Interleukin 3; Animals; Antineoplastic Agents; Cell Line Tumor; Cell Proliferation; Disease Models Animal; Drug Carriers; Exosomes; HEK293 Cells; Heterografts; Humans; Imatinib Mesylate; Leukemia Myelogenous Chronic BCR-ABL Positive; Mice; Receptors Interleukin-3; Treatment Outcome3. Good healthTreatment OutcomeImatinib MesylateHeterograftsHeterograftResearch Papermedicine.drugHumanEngineered exosomesAntineoplastic Agents03 medical and health sciencesIn vivoCell Line TumorLeukemia Myelogenous Chronic BCR-ABL PositivemedicineAnimalsHumansneoplasmsInterleukin 3.Interleukin 3Cell Proliferationbusiness.industryAnimalImatinibmedicine.diseaseMicrovesiclesReceptors Interleukin-3ExosomeDisease Models AnimalHEK293 Cells030104 developmental biologyImatinib mesylateDrug resistanceCancer cellDrug deliverybusinessChronic myelogenous leukemia
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Role of the HIPPO pathway as potential key player in the cross talk between oncology and cardiology.

2021

The HIPPO pathway (HP) is a highly conserved kinase cascade that affects organ size by regulating proliferation, cell survival and differentiation. Discovered in Drosophila melanogaster to early 2000, it immediately opened wide frontiers in the field of research. Over the last years the field of knowledge on HP is quickly expanding and it is thought will offer many answers on complex pathologies. Here, we summarized the results of several studies that have investigated HP signaling both in oncology than in cardiology field, with an overview on future perspectives in cardiology research.

0301 basic medicineOncologymedicine.medical_specialtyCardiologyProtein Serine-Threonine KinasesCardiac regeneration03 medical and health sciences0302 clinical medicineInternal medicinemedicineAnimalsHumansHippo Signaling PathwayCardio oncologyCell survivalCell ProliferationHippo signaling pathwaybiologybusiness.industryHematologybiology.organism_classificationKinase cascade030104 developmental biologyDrosophila melanogasterOncologyCardiology fieldAnimals Cardiac development Cardiac regeneration Cardio-oncology Cardiology Cell Proliferation Drosophila melanogaster HIPPO signaling pathway Humans Protein Serine-Threonine Kinases030220 oncology & carcinogenesisCardiologyDrosophila melanogasterbusinessSignal TransductionCritical reviews in oncology/hematology
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