Search results for "APOPTOSIS"

showing 10 items of 1809 documents

Silencing of C3G increases cardiomyocyte survival inhibition and apoptosis via regulation of p-ERK1/2 and Bax

2019

Experimental studies have shown that overexpression of Rap guanine nucleotide exchange factor 1 (C3G) plays pro‐survival and anti‐apoptotic roles through molecule phosphorylated extracellular signal‐regulated kinase1/2 (p‐ERK1/2) in cardiomyocytes. However, it is still unclear if silencing of C3G may increase cell survival inhibition and apoptosis in cardiomyocytes, and whether C3G silence induced injuries are reduced by the overexpression of C3G through regulation of p‐ERK1/2 and pro‐apoptotic molecule Bax. In this study, the rat‐derived H9C2 cardiomyocytes were infected with C3G small hairpin RNA interference recombinant lentiviruses, which silenced the endogenous C3G expression in the ca…

ohjelmoitunut solukuolemaBaxsydänapoptosiscardiac myocyteRap guanine nucleotide exchange factor 1proteiinithenkiinjääminenH9C2 cell linep-ERK1/2lihassolut
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Selection of the best three oocytes for intracytoplasmic sperm injection (ICSI) using apoptotic analysis of cumulus cells

2009

Introduction: We studied the apoptosis rate of the cumulus cells of individual cumulus-oocyte complex (COC), to verify a relationship with clinical outcomes, in terms of pregnancy and implantation rates. Usually oocytes are selected using morphological criteria. We tried to verify if cumulus cell apoptotic rate could be used as a molecular criteria in selecting oocytes with higher implantation potentiality. Material and Methods: The study design consisted in two different trials: in the first we investigated apoptosis rate in cumulus cells of the three selected oocytes, according to Italian law, to be fertilized by intracytoplasmic sperm injection (ICSI). In a second trial, average apoptosi…

oocytes ICSI apoptosis cumulus cellsSettore BIO/06 - Anatomia Comparata E Citologia
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Cell-cycle control in cell-biomaterial interactions

2000

Current biocompatibility testing involves the demonstration of cell proliferation, which is usually interpreted as a sign of positive biocompatibility when the materials sustain cell proliferation. As the field of biomaterials research is rapidly moving toward tissue-engineered devices and hybrid organs, control of cell function has become a main topic. Cell function, which involves specific differentiation pathways, cannot be separated from cell-cycle control. The study of cell-cycle control is an important extension of routine proliferation assays and has extensive roots in developmental and tumor biology. We studied the expression of the tumour suppressor gene p53 and the proliferation-a…

p53BiocompatibilityBiomedical EngineeringFOCAL ADHESION KINASEHUMAN BONEPROTEINBiologyFlow cytometryBiomaterialsFocal adhesionbiomaterials testing methodsmedicineKI-67BREAST-CANCERmedicine.diagnostic_testCell growthINDUCTIONPROLIFERATIONBiomaterialCell cycleCell biologyAPOPTOSISEndothelial stem cellFibronectinDNA-DAMAGEImmunologybiology.proteinendothelial cellcell cycleGROWTH ARRESTJournal of Biomedical Materials Research
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Apollon gene silencing induces apoptosis in breast cancer cells via p53 stabilisation and caspase-3 activation

2009

We analysed the effects of small interfering RNA (siRNA)-mediated silencing of Apollon, a member of the inhibitors of apoptosis protein family, on the proliferative potential and ability of human breast cancer cell lines to undergo apoptosis. In wild-type p53 ZR75.1 cells, Apollon knockdown resulted in a marked, time-dependent decline of cell growth and an increased rate of apoptosis, which was associated with p53 stabilisation and activation of the mitochondrial-dependent apoptotic pathway. Pre-incubation of cells with a p53-specific siRNA resulted in a partial rescue of cell growth inhibition, as well as in a marked reduction of the apoptotic response, indicating p53 as a major player in …

p53Cancer ResearchSmall interfering RNAProgrammed cell deathcaspase-3ApollonCaspase 3Breast NeoplasmsApollon gene apoptosisBiologyModels BiologicalInhibitor of Apoptosis ProteinsRNA interferenceTumor Cells CulturedGene silencingHumansGene SilencingRNA Small InterferingCell Proliferationhuman breast cancerGene knockdownCell growthCaspase 3Protein StabilityapoptosisEnzyme ActivationOncologyApoptosissiRNACancer researchSettore BIO/14 - FarmacologiaFemaleTumor Suppressor Protein p53Translational Therapeutics
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Endoderm development requires centrioles to restrain p53-mediated apoptosis in the absence of ERK activity

2021

Centrioles comprise the heart of centrosomes, microtubule-organizing centers. To study the function of centrioles in lung and gut development, we genetically disrupted centrioles throughout the mouse endoderm. Surprisingly, removing centrioles from the endoderm did not disrupt intestinal growth or development but blocked lung branching. In the lung, acentriolar SOX2-expressing airway epithelial cells apoptosed. Loss of centrioles activated p53, and removing p53 restored survival of SOX2-expressing cells, lung branching, and mouse viability. To investigate how endodermal p53 activation specifically killed acentriolar SOX2-expressing cells, we assessed ERK, a prosurvival cue. ERK was active t…

p53Cell SurvivalApoptosisInbred C57BLMedical and Health SciencesArticleGeneral Biochemistry Genetics and Molecular BiologyMiceMorphogenesis2.1 Biological and endogenous factorsAnimalscentrioleintestine developmentAetiologyExtracellular Signal-Regulated MAP KinasesendodermLungMolecular BiologyCentriolesSOXB1 Transcription FactorsStem CellsEndodermapoptosisEpithelial CellsCell BiologyBiological SciencesIntestinesMice Inbred C57BLlung branchingERKembryonic structuresTumor Suppressor Protein p53Microtubule-Associated ProteinsDevelopmental BiologyDevelopmental Cell
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Digital control circuitry for the p53 dynamics in cancer cell and apoptosis

2010

Abstract Experimental work and theoretical models deduce a “digital” response of the p53 transcription factor when genomic integrity is damaged. The mutual influence of p53 and its antagonist, the Mdm2 oncogene, is closed in a feedback. This paper proposes an aerospace-based architecture for translating the p53/Mdm2/DNA damage network into a digital circuitry in which the optimal control theory is applied for obtaining the requested dynamic evolutions of some considered cell species for repairing a DNA damage. The purpose of this paper is to demonstrate the usefulness of such digital circuitry design to detect and predict the cell species dynamics for shedding light on their inner and mutua…

p53General Immunology and MicrobiologyMechanism (biology)DNA damageQH301-705.5General NeuroscienceapoptosisWiring diagramCell fate determinationBiologycellular circuitryBioinformaticsOptimal controlGeneral Biochemistry Genetics and Molecular Biologyprotein networks signallingfeedback controlCancer cellDigital controlBiology (General)General Agricultural and Biological SciencesBiological systemTranscription factorOpen Life Sciences
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THE HDAC INHIBITOR ITF2357 (GIVINOSTAT) AS A KEY PLAYER IN EPIGENETIC TARGETING OF MELANOMA AND COLON CANCER CELLS

2023

Histone deacetylase inhibitors (HDACIs) are epigenetic compounds that have been recently considered for their promising anti-tumor activity. The aim of this PhD thesis was to elucidate and characterize the anti-tumor effect of the HDAC inhibitor ITF2357 (Givinostat) in melanoma and colon cancer cells that are characterized by oncogenic BRAF mutations. Interestingly, data reported in this thesis demonstrate that ITF2357 exerts a remarkable anti-tumor effect in melanoma cells by inducing a switch from a pro-survival autophagy to caspase-dependent apoptosis. The thesis provides the first evidences that ITF2357 is able to target oncogenic BRAF and oncogenic p53. The ITF2357 decreasing effect on…

p53HDAC inhibitorSettore BIO/10 - BiochimicaAutophagyEpigeneticApoptosisMelanomaColon cancerBRAF
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Oncogenic BRAF and p53 Interplay in Melanoma Cells and the Effects of the HDAC Inhibitor ITF2357 (Givinostat)

2023

Oncogenic BRAF mutations have been widely described in melanomas and promote tumour progression and chemoresistance. We previously provided evidence that the HDAC inhibitor ITF2357 (Givinostat) targets oncogenic BRAF in SK-MEL-28 and A375 melanoma cells. Here, we show that oncogenic BRAF localises to the nucleus of these cells, and the compound decreases BRAF levels in both the nuclear and cytosolic compartments. Although mutations in the tumour suppressor p53 gene are not equally frequent in melanomas compared to BRAF, the functional impairment of the p53 pathway may also contribute to melanoma development and aggressiveness. To understand whether oncogenic BRAF and p53 may cooperate, a po…

p53HDAC inhibitor; ITF2357; BRAF; melanoma; p53; apoptosisOrganic ChemistryapoptosisGeneral MedicineCatalysisComputer Science ApplicationsBRAFInorganic ChemistryHDAC inhibitorSettore BIO/10 - BiochimicaITF2357melanomaPhysical and Theoretical ChemistryMolecular BiologySpectroscopy
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TRAIL acts synergistically with iron oxide nanocluster-mediated magneto- and photothermia

2019

International audience; Targeting TRAIL (Tumor necrosis factor (TNF)-Related Apoptosis-Inducing Ligand) receptors for cancer therapy remains challenging due to tumor cell resistance and poor preparations of TRAIL or its derivatives. Herein, to optimize its therapeutic use, TRAIL was grafted onto iron oxide nanoclusters (NCs) with the aim of increasing its pro-apoptotic potential through nanoparticle-mediated magnetic hyperthermia (MHT) or photothermia (PT). Methods: The nanovector, NC@TRAIL, was characterized in terms of size, grafting efficiency, and potential for MHT and PT. The therapeutic function was assessed on a TRAIL-resistant breast cancer cell line, MDA-MB-231, wild type (WT) or T…

photothermal therapyCell SurvivalMedicine (miscellaneous)TRAIL02 engineering and technologyFerric CompoundsFlow cytometryTNF-Related Apoptosis-Inducing LigandCell membrane03 medical and health sciences0302 clinical medicineMicroscopy Electron TransmissionCell surface receptorCell Line Tumormedicine[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biologymagnetic hyperthermiaReceptorPharmacology Toxicology and Pharmaceutics (miscellaneous)ComputingMilieux_MISCELLANEOUSchemistry.chemical_classificationCell Deathmedicine.diagnostic_testTumor Necrosis Factor-alphairon oxide nanoclustersapoptosisHyperthermia InducedFlow Cytometry021001 nanoscience & nanotechnology3. Good healthMagnetic hyperthermiamedicine.anatomical_structurechemistryTransferrinApoptosis030220 oncology & carcinogenesisCancer research[SDV.IB]Life Sciences [q-bio]/BioengineeringTumor necrosis factor alpha0210 nano-technologyResearch Paper
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Adrb3 adrenergic receptor is a key regulator of human myometrial apoptosis and inflammation during chorioamnionitis1

2008

The pathophysiology underlying preterm labor triggered by inflammatory conditions such as chorioamnionitis remains largely unclear. It has already been suggested that beta-3 adrenergic (ADRB3) agonists might be of interest in the pharmacological management of preterm labor. Although there is evidence implicating ADRB receptors in the control of inflammation, there are minimal data relating specifically to ADRB3. To explore the cellular consequences of chorioamnionitis and detect apoptosis, we first performed immunostaining and Western blot experiments on human myometrial samples obtained from women with confirmed chorioamnionitis. We then developed an in vitro model of chorioamnionitis by i…

preterm labormedicine.medical_specialtymedicine.medical_treatmentunited-statesbeta-adrenoceptorsStimulationInflammationin-vitroChorioamnionitisProinflammatory cytokineimmunology03 medical and health sciences0302 clinical medicineInternal medicinemedicineInterleukin 8Interleukin 6030304 developmental biology0303 health sciencesbiologycell apoptosislipopolysaccharideapoptosisbacterial infectionCell BiologyGeneral Medicinemedicine.diseasegene-expressioncytokines3. Good healthEndocrinologyCytokineReproductive Medicineinflammation030220 oncology & carcinogenesisbiology.proteincytokine productionbeta(3)-adrenoceptorTumor necrosis factor alphapregnancymedicine.symptomdeliverytumor-necrosis-factorterm
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