Search results for "Apoptosis ."

showing 10 items of 177 documents

MYCN and survivin cooperatively contribute to malignant transformation of fibroblasts

2013

The oncogenes MYCN and survivin (BIRC5) maintain aggressiveness of diverse cancers including sarcomas. To investigate whether these oncogenes cooperate in initial malignant transformation, we transduced them into Rat-1 fibroblasts. Indeed, survivin enhanced MYCN-driven contact-uninhibited and anchorage-independent growth in vitro. Importantly, upon subcutaneous transplantation into mice, cells overexpressing both instead of either one of the oncogenes generated tumors with shortened latency, marked anaplasia and an increased proliferation-to-apoptosis ratio resulting in accelerated growth. Mechanistically, the increased tumorigenicity was associated with an enhanced Warburg effect and a hyp…

Cancer ResearchSurvivinBlotting WesternApoptosisBiologyReal-Time Polymerase Chain ReactionN-Myc Proto-Oncogene ProteinInhibitor of Apoptosis ProteinsMalignant transformationImmunoenzyme TechniquesMiceAdenosine TriphosphateSurvivinmedicineAnimalsHumansLactic AcidRNA MessengerneoplasmsAnaplasiaCells CulturedCell ProliferationHomeodomain ProteinsOncogene ProteinsN-Myc Proto-Oncogene ProteinReverse Transcriptase Polymerase Chain ReactionCell growthNuclear ProteinsGeneral MedicineFibroblastsWarburg effectCell HypoxiaRatsTransplantationCell Transformation NeoplasticGlucoseHypoxia-inducible factorsCancer researchmedicine.symptomGlycolysisCarcinogenesis
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Apoptosis: focus on sea urchin development

2009

It has been proposed that the apoptosis is an essential requirement for the evolution of all animals, in fact the apoptotic program is highly conserved from nematodes to mammals. Throughout development, apoptosis is employed by multicellular organisms to eliminate damaged or unnecessary cells. Here, we will discuss both developmental programmed cell death (PCD) under normal conditions and stress induced apoptosis, in sea urchin embryos. Sea urchin represent an excellent model system for studying embryogenesis and cellular processes involved in metamorphosis. PCD plays an essential role in sculpting and remodelling the embryos and larvae undergoing metamorphosis. Moreover, this marine organi…

Cancer Researchanimal structuresmedia_common.quotation_subjectClinical BiochemistryDefence mechanismsPharmaceutical ScienceApoptosisEmbryos PCD Stress CaspasesApoptosis evolution EchinodermsEvolution Molecularbiology.animalAnimalsSettore BIO/06 - Anatomia Comparata E CitologiaMetamorphosisSea urchinCaspasemedia_commonPharmacologybiologyEcologyBiochemistry (medical)EmbryogenesisEmbryoCell BiologyCell biologyMulticellular organismApoptosisSea Urchinsembryonic structuresbiology.proteinApoptosis
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Parthenolide generates reactive oxygen species and autophagy in MDA-MB231 cells. A soluble parthenolide analogue inhibits tumour growth and metastasi…

2013

Triple-negative breast cancers (TNBCs) are clinically aggressive forms associated with a poor prognosis. We evaluated the cytotoxic effect exerted on triple-negative MDA-MB231 breast cancer cells both by parthenolide and its soluble analogue dimethylamino parthenolide (DMAPT) and explored the underlying molecular mechanism. The drugs induced a dose- and time-dependent decrement in cell viability, which was not prevented by the caspase inhibitor z-VAD-fmk. In particular in the first hours of treatment (1–3 h), parthenolide and DMAPT strongly stimulated reactive oxygen species (ROS) generation. The drugs induced production of superoxide anion by activating NADPH oxidase. ROS generation caused…

Cancer ResearchautophagyCell SurvivalparthenolideFas-Associated Death Domain ProteinImmunologyCASP8 and FADD-Like Apoptosis Regulating ProteinBreast Neoplasmsparthenolide; ROS; NOX; autophagy; breast cancer xenograft.MiceCellular and Molecular Neurosciencechemistry.chemical_compoundDownregulation and upregulationCell Line TumorSettore BIO/10 - BiochimicaAnimalsHumansParthenolidePropidium iodidebreast cancer xenograftMembrane Potential Mitochondrialchemistry.chemical_classificationReactive oxygen speciesNADPH oxidasebiologybreast cancer xenograft.SuperoxideNF-kappa BRNA-Binding ProteinsROSCell BiologyNOXXenograft Model Antitumor AssaysMolecular biologyNuclear Pore Complex ProteinsVascular endothelial growth factorchemistryCell cultureCancer researchbiology.proteinCalciumFemaleOriginal ArticleReactive Oxygen SpeciesSesquiterpenes
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Immune escape of AKT overexpressing ovarian cancer cells

2012

Platinum-resistance is the most crucial problem for treatment of ovarian cancer. There is a clinical need for new treatment strategies which overcome platinum resistance. As survival is strongly influenced by immunological parameters, immunotherapeutic strategies appear promising. Therefore a better understanding of the interaction between ovarian tumour cells and cells of the immune system is a necessary prerequisite. In the present study we aimed to enlighten the interactions between platinum resistant and platinum sensitive ovarian cancer cells and natural-killer (NK)-cells. Modified FATAL assay was used for determining the killing efficiency of NK-cells for the parental A2780 cells and …

Cancer Researchendocrine system diseasesUbiquitin-Protein LigasesCellApoptosisBiologymedicine.disease_causeInhibitor of Apoptosis ProteinsImmune systemCell Line TumormedicineHumansPlatinumOvarian NeoplasmsCancerCell cyclemedicine.diseaseBaculoviral IAP Repeat-Containing 3 Proteinfemale genital diseases and pregnancy complicationsGene Expression Regulation NeoplasticKiller Cells Naturalmedicine.anatomical_structureOncologyDrug Resistance NeoplasmCell cultureApoptosisCancer researchFemaleOvarian cancerCarcinogenesisProto-Oncogene Proteins c-aktInternational Journal of Oncology
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Cyclooxygenase-2 inhibition induces apoptosis signaling via death receptors and mitochondria in hepatocellular carcinoma.

2006

AbstractInhibition of cyclooxygenase (COX)-2 elicits chemopreventive and therapeutic effects in solid tumors that are coupled with the induction of apoptosis in tumor cells. We investigated the mechanisms by which COX-2 inhibition induces apoptosis in hepatocellular carcinoma (HCC) cells. COX-2 inhibition triggered expression of the CD95, tumor necrosis factor (TNF)-R, and TNF-related apoptosis-inducing ligand (TRAIL)-R1 and TRAIL-R2 death receptors. Addition of the respective specific ligands further increased apoptosis, indicating that COX-2 inhibition induced the expression of functional death receptors. Overexpression of a dominant-negative Fas-associated death domain mutant reduced COX…

Cancer Researchmedicine.medical_specialtyProgrammed cell deathCarcinoma HepatocellularApoptosisMitochondria LiverBiologyTransfectionReceptors Tumor Necrosis FactorInternal medicineCell Line TumormedicineHumansfas ReceptorDeath domainInhibitor of apoptosis domainSulfonamidesCyclooxygenase 2 InhibitorsIntrinsic apoptosisLiver NeoplasmsFas receptorReceptors TNF-Related Apoptosis-Inducing LigandEndocrinologyOncologyUVB-induced apoptosisApoptosisCelecoxibCyclooxygenase 2Cancer researchPyrazolesSignal transductionSignal TransductionCancer research
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Autocrine production of interleukin-4 and interleukin-10 is required for survival and growth of thyroid cancer cells.

2006

AbstractAlthough CD95 and its ligand are expressed in thyroid cancer, the tumor cell mass does not seem to be affected by such expression. We have recently shown that thyroid carcinomas produce interleukin (IL)-4 and IL-10, which promote resistance to chemotherapy through the up-regulation of Bcl-xL. Here, we show that freshly purified thyroid cancer cells were completely refractory to CD95-induced apoptosis despite the consistent expression of Fas-associated death domain and caspase-8. The analysis of potential molecules able to prevent caspase-8 activation in thyroid cancer cells revealed a remarkable up-regulation of cellular FLIPL (cFLIPL) and PED/PEA-15, two antiapoptotic proteins whos…

Cancer Researchmedicine.medical_treatmentNF-KAPPA-BOligonucleotidesC-FLIPCASP8 and FADD-Like Apoptosis Regulating ProteinApoptosisSuppressor of Cytokine Signaling ProteinsSIGNALING COMPLEXThyroid cancerTumorCARCINOMA CELLSANDROGEN RECEPTORIntracellular Signaling Peptides and ProteinsInterleukinHASHIMOTOS-THYROIDITISMiddle AgedProtein-Tyrosine KinasesInterleukin-10Up-RegulationMALIGNANT GLIOMA-CELLSInterleukin 10CytokineOncologyAged; Antibodies; Apoptosis; CASP8 and FADD-Like Apoptosis Regulating Protein; Cell Growth Processes; Cell Line Tumor; Humans; Interleukin-10; Interleukin-4; Intracellular Signaling Peptides and Proteins; Janus Kinase 1; Middle Aged; Oligonucleotides Antisense; Phosphoproteins; Protein-Tyrosine Kinases; Repressor Proteins; STAT6 Transcription Factor; Suppressor of Cytokine Signaling 1 Protein; Suppressor of Cytokine Signaling Proteins; Thyroid Neoplasms; Up-Regulation; fas Receptor; Oncology; Cancer Researchmedicine.medical_specialtyANTIAPOPTOTIC PROTEINSCell Growth ProcessesAntibodiesCell LineThyroid carcinomaSuppressor of Cytokine Signaling 1 ProteinSettore MED/04 - PATOLOGIA GENERALEInternal medicineCell Line TumormedicineHumansThyroid Neoplasmsfas ReceptorAntisenseAutocrine signallingInterleukin 4AgedAPOPTOSIS-INDUCING LIGANDbusiness.industryJanus Kinase 1Oligonucleotides Antisensemedicine.diseasePhosphoproteinsRepressor ProteinsEndocrinologyCancer cellCancer researchInterleukin-4businessApoptosis Regulatory ProteinsSTAT6 Transcription FactorCancer research
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Apoptosis induced in HepG2 cells by the synthetic cannabinoid WIN: involvement of the transcription factor PPARgamma.

2008

It has recently been shown that cannabinoids induce growth inhibition and apoptosis in different tumour cell lines. In the current study, the effects of WIN 55,212-2 (WIN), a synthetic and potent cannabinoid receptor agonist, are investigated in hepatoma HepG2 cells and a possible signal transduction pathway is proposed. In these cells, WIN induces a clear apoptotic effect which was accompanied by up-regulation of the death-signalling factors Bax, Bcl-X(S), t-Bid and down-regulation of the survival factors survivin, phospho-AKT, Hsp72 and Bcl-2. Moreover, WIN-induced apoptosis is associated with JNK/p38 MAPK pathway activation and mitochondrial depolarisation demonstrated by a cytofluorimet…

Cannabinoid receptorCarcinoma HepatocellularCell SurvivalPyridinesmedicine.medical_treatmentp38 mitogen-activated protein kinasesMorpholinesApoptosisBiologyNaphthalenesBiochemistryReceptor Cannabinoid CB2Membrane Microdomainscannabinoids PPARgamma factor apoptosis cancer cellsSettore BIO/10 - BiochimicaCell Line TumorSurvivinmedicineHumansAnilidesViability assayCannabinoidsLiver NeoplasmsGeneral MedicineCell biologyBenzoxazinesPPAR gammaApoptosisCancer cellBenzamidesCannabinoidSignal transductionApoptosis Regulatory ProteinsProtein KinasesSignal TransductionBiochimie
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Cannabinoid receptor 1 modulates the autophagic flux independent of mTOR- and BECLIN1-complex

2013

Cannabinoid Receptor 1 (CB1) has been initially described as the receptor for Delta-9-Tetrahydrocannabinol in the central nervous system (CNS), mediating retrograde synaptic signaling of the endocannabinoid system. Beside its expression in various CNS regions, CB1 is ubiquituous in peripheral tissues, where it mediates, among other activities, the cell's energy homeostasis. We sought to examine the role of CB1 in the context of the evolutionarily conserved autophagic machinery, a main constituent of the regulation of the intracellular energy status. Manipulating CB1 by siRNA knockdown in mammalian cells caused an elevated autophagic flux, while the expression of autophagy-related genes rema…

Cannabinoid receptorMorpholinesGreen Fluorescent ProteinsDown-RegulationmTORC1NaphthalenesBiochemistryMiceCellular and Molecular NeurosciencePiperidinesReceptor Cannabinoid CB1RimonabantAutophagymedicineAnimalsHumansEnzyme InhibitorsCannabinoid Receptor AntagonistsCells CulturedPI3K/AKT/mTOR pathwayAdenine NucleotidesChemistryTOR Serine-Threonine KinasesAutophagyMembrane ProteinsCalcium Channel BlockersEmbryo MammalianEndocannabinoid systemBenzoxazinesCell biologyMice Inbred C57BLnervous systemAstrocytesPyrazolesBeclin-1lipids (amino acids peptides and proteins)MacrolidesSynaptic signalingRimonabantApoptosis Regulatory ProteinsFlux (metabolism)medicine.drugJournal of Neurochemistry
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Expression of IAPs and alternative splice variants in hepatocellular carcinoma tissues and cells.

2005

IAPs (inhibitors of apoptosis proteins) might have a major role in the apoptotic resistance that marks many cancers. The studies on IAPs in human HCC have focused on survivin or XIAP, indicating that their new or increased expression in this tumor is associated with a more unfavorable prognosis. The present results corroborate these findings, emphasizing the role that the coordinated expression of different IAPs and alternative splice variants might play in the adverse biology of hepatocellular carcinoma.

Carcinoma HepatocellularApoptosisX-Linked Inhibitor of Apoptosis ProteinBiologyBioinformaticsGeneral Biochemistry Genetics and Molecular BiologyHistory and Philosophy of ScienceCell Line TumorSurvivinCarcinomamedicineHumansspliceRNA MessengerCell ProliferationCell growthReverse Transcriptase Polymerase Chain ReactionGeneral NeuroscienceAlternative splicingLiver NeoplasmsIntracellular Signaling Peptides and ProteinsProteinsmedicine.diseasePrognosisXIAPbody regionsAlternative SplicingApoptosisDrug Resistance NeoplasmHepatocellular carcinomaCancer researchAnnals of the New York Academy of Sciences
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Genome-wide association analysis in dilated cardiomyopathy reveals two new players in systolic heart failure on chromosomes 3p25.1 and 22q11.23

2021

Abstract Aims  Our objective was to better understand the genetic bases of dilated cardiomyopathy (DCM), a leading cause of systolic heart failure. Methods and results  We conducted the largest genome-wide association study performed so far in DCM, with 2719 cases and 4440 controls in the discovery population. We identified and replicated two new DCM-associated loci on chromosome 3p25.1 [lead single-nucleotide polymorphism (SNP) rs62232870, P = 8.7 × 10−11 and 7.7 × 10−4 in the discovery and replication steps, respectively] and chromosome 22q11.23 (lead SNP rs7284877, P = 3.3 × 10−8 and 1.4 × 10−3 in the discovery and replication steps, respectively), while confirming two previously identif…

Cardiac & Cardiovascular SystemsCardiomyopathy Dilated/genetics[SDV]Life Sciences [q-bio]Signal Transducing/geneticsDilated cardiomyopathyGenome-wide association studyAdaptor Proteins Signal Transducing/genetics030204 cardiovascular system & hematologyTAURINE0302 clinical medicineGWASMedicinePOSITION STATEMENT1102 Cardiorespiratory Medicine and HaematologyGenetics0303 health scienceseducation.field_of_studyGenetic Predisposition to Disease/geneticsAdaptor ProteinsDilated cardiomyopathy4C-sequencingPolymorphism Single Nucleotide/geneticsGenetic risk scoreCardiology and Cardiovascular MedicineLife Sciences & BiomedicineSingle Nucleotide/geneticsCardiomyopathy DilatedCardiomyopathyPopulationLocus (genetics)Single-nucleotide polymorphismPolymorphism Single NucleotideChromosomes03 medical and health sciencesSystolic/geneticsHeart Failure Systolic/geneticsSNPAnimalsHumansGenetic Predisposition to DiseaseAllelePolymorphismeducationImputationAdaptor Proteins Signal Transducing030304 developmental biologyHeart FailureScience & Technologybusiness.industryWORKING GROUP1103 Clinical Sciencesmedicine.diseaseGenetic architectureCardiovascular System & Hematology Dilated cardiomyopathyDilated/geneticsCardiovascular System & Cardiology[SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologiebusinessApoptosis Regulatory ProteinsHeart Failure SystolicGenome-Wide Association Study
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