Search results for " Mitogen"

showing 10 items of 202 documents

Midregion PTHrP regulates Rip1 and caspase expression in MDA-MB231 breast cancer cells.

2007

It was previously reported that the midregion PTHrP domain (38-94)-amide restrains growth and invasion "in vitro", causes striking toxicity and accelerates death of some breast cancer cell lines, the most responsive being MDA-MB231 whose tumorigenesis was also attenuated "in vivo". In addition, we have demonstrated that midregion PTHrP is imported in the nucleoplasm of cultured MDA-MB231 cells, and that "in vitro" it can bind chromatin of metaphase spread preparations and also an isolated 20-mer oligonucleotide, thereby appearing endowed with a putative transcription factor-like DNA-binding ability. Here, we examined whether PTHrP (38-94)-amide was able to modulate the expression of genes e…

Cancer ResearchProgrammed cell deathbcl-X ProteinApoptosisBreast NeoplasmsPTHrP Rip1 caspase breast cancer cellsmedicine.disease_causeTransfectionCell MovementCell Line TumorGene expressionmedicineTranscriptional regulationHumansNeoplasm InvasivenessSettore BIO/06 - Anatomia Comparata E Citologiaskin and connective tissue diseasesCaspaseCell ProliferationNucleoplasmbiologyJNK Mitogen-Activated Protein KinasesParathyroid Hormone-Related ProteinRNA-Binding ProteinsOligonucleotides AntisenseMolecular biologyPeptide FragmentsChromatinCell biologyNuclear Pore Complex ProteinsSettore BIO/12 - Biochimica Clinica E Biologia Molecolare ClinicaOncologyApoptosisCaspasesbiology.proteinFemalebcl-Associated Death ProteinCarcinogenesisSignal TransductionBreast cancer research and treatment
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The role of oxidative stress in apoptosis induced by the histone deacetylase inhibitor suberoylanilide hydroxamic acid in human colon adenocarcinoma …

2008

Histone deacetylase inhibitors (HDACIs) activate genes that promote cell cycle arrest and apoptosis in a number of tumor cells. This study showed that suberoylanilide hydroxamic acid (SAHA), a potent and commonly used HDACI, induced apoptosis in human colon adenocarcinoma HT-29 cells in a time- and dose-dependent manner. This effect was accompanied by the induction of oxidative stress, dissipation of mitochondrial transmembrane potential and activation of executioner caspases. Moreover, SAHA increased the levels of phosphorylated active forms of p38 and JNK. The addition of either the antioxidant N-acetylcysteine or the specific inhibitor of NADPH oxidase diphenylene iodonium chloride reduc…

Cancer ResearchProgrammed cell deathmedicine.drug_classCell Survivalp38 mitogen-activated protein kinasesBlotting WesternApoptosisAdenocarcinomamedicine.disease_causeHydroxamic AcidsAntioxidantsSettore BIO/10 - BiochimicamedicineHumansEnzyme InhibitorsProtein kinase BCaspaseMembrane Potential MitochondrialVorinostatbiologyHistone deacetylase inhibitorEnzyme ActivationHistone Deacetylase InhibitorsOxidative StressOncologyBiochemistryApoptosisCaspasesColonic NeoplasmsCancer researchbiology.proteinHistone deacetylaseReactive Oxygen Speciescolon adenomacarcinoma cells histone deacetylase inhibitors apoptosisHT29 CellsOxidative stressSignal TransductionInternational journal of oncology
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Pharmacological targeting of the novel β-catenin chromatin-associated kinase p38α in colorectal cancer stem cell tumorspheres and organoids

2021

AbstractThe prognosis of locally advanced colorectal cancer (CRC) is currently unsatisfactory. This is mainly due to drug resistance, recurrence, and subsequent metastatic dissemination, which are sustained by the cancer stem cell (CSC) population. The main driver of the CSC gene expression program is Wnt signaling, and previous reports indicate that Wnt3a can activate p38 MAPK. Besides, p38 was shown to feed into the canonical Wnt/β-catenin pathway. Here we show that patient-derived locally advanced CRC stem cells (CRC-SCs) are characterized by increased expression of p38α and are “addicted” to its kinase activity. Of note, we found that stage III CRC patients with high p38α levels display…

Cancer ResearchSettore MED/06 - Oncologia Medicapost-translationalImmunologyPopulationSynthetic lethalityArticleCellular and Molecular NeuroscienceCancer stem cellchromatin; colorectal neoplasms; humans; mitogen-activated protein kinase 14; neoplastic stem cells; organoids; prognosis; protein processing post-translational; beta cateninMedicineKinase activitycolon cancer p38 cancer stem cellslcsh:QH573-671educationhumansmitogen-activated protein kinase 14organoidsTrametinibSettore MED/04 - Patologia Generaleeducation.field_of_studybusiness.industrylcsh:CytologyCancer stem cellsneoplastic stem cellsWnt signaling pathwayprotein processingCell Biologycolorectal neoplasmsColorectal cancerdigestive system diseasesSettore BIO/12 - Biochimica Clinica E Biologia Molecolare ClinicaCateninCancer researchbeta cateninchromatinprognosisStem cellSettore MED/46 - Scienze Tecniche Di Medicina Di LaboratoriobusinessProtein Processing Post-TranslationalPost-translational modifications
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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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Transcriptional and post-transcriptional regulation of iNOS expression in human chondrocytes

2009

Chondrocytes are important for the development and maintenance of articular cartilage. However, both in osteoarthritis (OA) and rheumatoid arthritis (RA) chondrocytes are involved in the process of cartilage degradation and synthesize important immunomodulatory mediators, including nitric oxide (NO) generated by the inducible NO synthase (iNOS). To uncover the role of iNOS in the pathomechanisms of OA and RA, we analyzed the regulation of iNOS expression using immortalized human chondrocytes as a reproducible model. In C-28/I2 chondrocytes, iNOS expression was associated with the expression of the chondrocyte phenotype. Peak induction by a cytokine cocktail occurred between 6 and 8h and dec…

Cartilage Articularmedicine.medical_specialtyAnti-Inflammatory AgentsNitric Oxide Synthase Type IIBiologyBiochemistryp38 Mitogen-Activated Protein KinasesChondrocyteArticleGene Expression Regulation EnzymologicGlucocorticoid receptorChondrocytesReceptors GlucocorticoidInternal medicineGene expressionmedicineHumansRNA MessengerRNA Processing Post-TranscriptionalPost-transcriptional regulationCell Line TransformedPharmacologyRegulation of gene expressionNF-kappa B p50 SubunitRNA-Binding ProteinsInterferon-Stimulated Gene Factor 3Janus Kinase 2Cell biologyNitric oxide synthaseEndocrinologymedicine.anatomical_structureCell cultureEnzyme Inductionbiology.proteinTrans-ActivatorsCytokinesZearalenoneSignal transduction
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Cigarette Smoke Extract Induces p38 MAPK-Initiated, Fas-Mediated Eryptosis

2022

Eryptosis is a physiological mechanism for the clearance of senescent or damaged erythrocytes by phagocytes. Excessive eryptosis is stimulated under several pathologies and associated with endothelial injury and thrombosis. Cigarette smoke (CS) is an established risk factor for vascular diseases and cigarette smokers have high-levels of eryptotic erythrocytes. This study, for the first time, investigates the mechanism by which CS damages red blood cells (RBCs). CS extract (CSE) from commercial cigarettes was prepared and standardized for nicotine content. Cytofluorimetric analysis demonstrated that treatment of human RBCs with CSE caused dose-dependent, phosphatidylserine externalization an…

Caspase 8ErythrocytesCaspase 3cigarette smokeOrganic ChemistryGeneral Medicinep38 MAPKCeramidesp38 Mitogen-Activated Protein KinasesCatalysisComputer Science ApplicationsInorganic Chemistryeryptosis; cigarette smoke; death-inducing signaling complex (DISC); p38 MAPK; ceramide; caspasescaspasesSmokeeryptosisSettore BIO/10 - BiochimicaTobaccodeath-inducing signaling complex (DISC)HumansceramidePhysical and Theoretical ChemistryReactive Oxygen SpeciesMolecular BiologySpectroscopy
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Cisplatin sensitivity is related to late DNA damage processing and checkpoint control rather than to the early DNA damage response

2008

The present study aimed at elucidating mechanisms dictating cell death triggered by cisplatin-induced DNA damage. We show that CL-V5B hamster mutant cells, a derivative of V79B, are hypersensitive to cisplatin-induced apoptotic death. CL-V5B cells are characterized by attenuated cisplatin-induced early (2-6 h) stress response, such as phosphorylation of stress-activated protein kinases (SAPK/JNK), ATM and Rad3-related (ATR) protein kinase, histone H2AX and checkpoint kinase-1 (Chk-1). Human FANCC cells also showed a reduced phosphorylation of H2AX and SAPK/JNK at early time point after cisplatin treatment. This was not the case for BRCA2-defective VC-8 hamster cells, indicating that the FA …

Cell cycle checkpointCisplatin-DNA adducts ; DNA repair ; Interstrand cross links ; DNA damage response ; Cell cycle checkpoint ; Cell deathDNA damageDNA repairHealth Toxicology and MutagenesisApoptosisCell LineHistonesDNA AdductsCricetinaeGeneticsmedicineAnimalsHumansCHEK1PhosphorylationMolecular BiologyChromosome AberrationsCisplatinbiologyJNK Mitogen-Activated Protein KinasesDNA replicationG2-M DNA damage checkpointMolecular biologyCell biologyHistonebiology.proteinCisplatinDNA DamageMutagensmedicine.drug
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Distinct Signaling Cascades of TREM-1, TLR and NLR in Neutrophils and Monocytic Cells

2013

Triggering receptor expressed on myeloid cells 1 (TREM-1) is an important mediator of innate inflammatory responses in microbial infections and sepsis. TREM-1 ligation on neutrophils (PMN) or monocytes results in the production of proinflammatory cytokines. Engagement of TREM-1 induces the activation of MAP kinases as well as rapid Ca<sup>2+</sup> mobilization. However, a detailed understanding of TREM-1 signaling pathways is currently lacking. We evaluated the TREM-1 signaling hierarchy in monocytic cells and found that the acute myeloid leukemia cell line MUTZ-3 expresses TREM-1 in a natural and functional manner. We compared essential signaling molecules of the TREM-1, TLR an…

Cell signalingMyeloidNeutrophilsp38 Mitogen-Activated Protein KinasesMonocytesProinflammatory cytokinePhosphatidylinositol 3-KinasesCell Line TumormedicineHumansImmunology and AllergyCalcium SignalingReceptors ImmunologicExtracellular Signal-Regulated MAP KinasesPI3K/AKT/mTOR pathwayCalcium signalingMembrane GlycoproteinsChemistryToll-Like ReceptorsMyeloid leukemiaImmunity InnateTriggering Receptor Expressed on Myeloid Cells-1Cell biologyLeukemia Myeloid Acutemedicine.anatomical_structureOrgan SpecificityCell cultureImmunologyCytokinesInflammation MediatorsSignal transductionResearch ArticleJournal of Innate Immunity
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Mechanisms of ceramide-induced COX-2-dependent apoptosis in human ovarian cancer OVCAR-3 cells partially overlapped with resveratrol.

2013

Ceramide is a member of the sphingolipid family of bioactive molecules demonstrated to have profound, diverse biological activities. Ceramide is a potential chemotherapeutic agent via the induction of apoptosis. Exposure to ceramide activates extracellular-signal-regulated kinases (ERK)1/2- and p38 kinase-dependent apoptosis in human ovarian cancer OVCAR-3 cells, concomitant with an increase in the expression of COX-2 and p53 phosphorylation. Blockade of cyclooxygenase-2 (COX-2) activity by siRNA or NS398 correspondingly inhibited ceramide-induced p53 Ser-15 phosphorylation and apoptosis; thus COX-2 appears at the apex of the p38 kinase-mediated signaling cascade induced by ceramide. Induct…

CeramideMAP Kinase Signaling Systemp38 mitogen-activated protein kinasesApoptosisBiologyResveratrolCeramidesBiochemistryp38 Mitogen-Activated Protein KinasesGene Expression Regulation Enzymologicchemistry.chemical_compoundCell Line TumorStilbenesHumansPhosphorylationRNA Small InterferingMolecular BiologyNitrobenzenesCaspase 7Membrane Potential MitochondrialOvarian NeoplasmsSulfonamidesKinaseCaspase 3Anti-Inflammatory Agents Non-SteroidalCell BiologyLipid signalingSphingolipidCell biologyGene Expression Regulation NeoplasticchemistryApoptosisCyclooxygenase 2ResveratrolFemaleSignal transductionTumor Suppressor Protein p53Journal of cellular biochemistry
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Anandamide-induced apoptosis in Chang liver cells involves ceramide and JNK/AP-1 pathway

2006

In the present study we demonstrate that anandamide, the most important endogenous cannabinoid, markedly induced apoptosis in Chang liver cells, an immortalized non-tumor cell line derived from normal liver tissue, while it induced only modest effects in a number of hepatoma cell lines. The apoptotic effect was reduced by methyl-beta-cyclodextrin, a membrane cholesterol depletor, suggesting an interaction between anandamide and the membrane microdomains named lipid rafts. Anandamide effects were mediated by the production of ceramide, as demonstrated by experiments performed with the sphingomyelinase inhibitor, desipramine, or with the sphingomyelinase activator, melittin. This conclusion w…

CeramideProgrammed cell deathFas Ligand ProteinCell SurvivalPolyunsaturated AlkamidesLiver cytologyp38 mitogen-activated protein kinasesBlotting WesternApoptosisArachidonic AcidsBiologyCeramidesCell LineMembrane Potentialschemistry.chemical_compoundCell Line TumorProto-Oncogene ProteinsGeneticsHumansEnzyme InhibitorsMembrane GlycoproteinsBcl-2-Like Protein 11Dose-Response Relationship DrugDesipramineJNK Mitogen-Activated Protein KinasesMembrane ProteinsFree Radical ScavengersGeneral MedicineAnandamideEndocannabinoid systemAcetylcysteineCell biologyEnzyme ActivationTranscription Factor AP-1cannabinoids apoptosis tumor cells JNK/AP1LiverchemistryApoptosisCaspasesMitochondrial MembranesTumor Necrosis FactorsApoptosis Regulatory ProteinsSphingomyelinEndocannabinoidsSignal TransductionInternational Journal of Molecular Medicine
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