Search results for "proliferation"

showing 10 items of 1193 documents

A petrol ether extract of the roots of Onosma paniculatum induces cell death in a caspase dependent manner

2010

Traditional Chinese medicine (TCM) has become very popular in Western countries during the last years. Zicao, a remedy of TCM, has been traditionally used to treat cancer, and, its main constituents, naphthoquinones, have been reported to possess antitumor activity (Chen et al., 2002; Papageorgiou et al., 1999). Here, we prepared extracts of different polarities of Onosma paniculatum Bur.Franch., a plant which is amongst others used as Zicao, but, much less investigated. The extracts were analyzed concerning their growth inhibitory and apoptosis-inducing activity in various tumor cells.Cell viability was measured by XTT viability and a growth inhibition assay. Effects on the cell cycle and …

Programmed cell deathDependent mannerApoptosisOnosma paniculatumGrowth inhibitoryEtherCaspase 3Traditional Chinese medicinePharmacologyEtherPlant Rootschemistry.chemical_compoundCell Line TumorNeoplasmsDrug DiscoveryHumansCaspaseCell ProliferationPharmacologyDose-Response Relationship DrugbiologyCaspase 3Cell CycleBoraginaceaeAntineoplastic Agents Phytogenicchemistrybiology.proteinDrugs Chinese HerbalPhytotherapyJournal of Ethnopharmacology
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Role of caspase-8 in hepatocyte response to infection and injury in mice.

2007

Caspase-8 has been implicated in signaling for apoptotic cell death and for certain nonapoptotic functions. However, knowledge of actual physiological or pathophysiological processes to which this enzyme contributes is lacking. Using a mouse model and employing the conditional knockout approach to delete the caspase-8 gene specifically in the liver, we found that caspase-8 deficiency in hepatocytes facilitates infection of the liver by Listeria monocytogenes, attenuates the hepatocyte proliferation wave during the first 48 hours after partial hepatectomy and, depending on the genetic background of the mice, prompts a chronic inflammatory response to the hepatectomy, as a result of which the…

Programmed cell deathInflammationCaspase 8MiceConditional gene knockoutmedicineAnimalsListeriosisCaspaseCell ProliferationInflammationMice KnockoutCaspase 8HepatologybiologyCell DeathCell growthLiver Regenerationmedicine.anatomical_structureHepatocyteImmunologyCancer researchChronic inflammatory responsebiology.proteinHepatocytesmedicine.symptomHepatology (Baltimore, Md.)
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Hypoxia inducible factor-1alpha inactivation unveils a link between tumor cell metabolism and hypoxia-induced cell death.

2008

Hypoxia and the acquisition of a glycolytic phenotype are intrinsic features of the tumor microenvironment. The hypoxia inducible factor-1alpha (HIF-1alpha) pathway is activated under hypoxic conditions and orchestrates a complex transcriptional program that enhances cell survival. Although the consequences of HIF-1alpha inactivation in cancer cells have been widely investigated, only a few studies have addressed the role of HIF-1alpha in the survival of cancer cells endowed with different glycolytic capacities. In this study, we investigated this aspect in ovarian cancer cells. Hypoxia-induced toxicity was increased in highly glycolytic cells compared with poorly glycolytic cells; it was a…

Programmed cell deathMice SCIDBiologyPathology and Forensic MedicineMiceCell Line TumormedicineAnimalsHumansGene SilencingRNA Small InterferingCell ProliferationOvarian NeoplasmsTumor microenvironmentCell DeathCell growthLentivirusHypoxia (medical)Hypoxia-Inducible Factor 1 alpha SubunitCell HypoxiaCell biologyPhenotypeHypoxia-inducible factorsApoptosisCell cultureCancer cellFemalemedicine.symptomRegular ArticlesThe American journal of pathology
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ROS-Dependent ER Stress and Autophagy Mediate the Anti-Tumor Effects of Tributyltin (IV) Ferulate in Colon Cancer Cells

2020

Organotin compounds represent potential cancer therapeutics due to their pro-apoptotic action. We recently synthesized the novel organotin ferulic acid derivative tributyltin (IV) ferulate (TBT-F) and demonstrated that it displays anti-tumor properties in colon cancer cells related with autophagic cell death. The purpose of the present study was to elucidate the mechanism of TBT-F action in colon cancer cells. We specifically show that TBT-F-dependent autophagy is determined by a rapid generation of reactive oxygen species (ROS) and correlated with endoplasmic reticulum (ER) stress. TBT-F evoked nuclear factor erythroid-2 related factor 2 (Nrf2)-mediated antioxidant response and Nrf2 silenc…

Programmed cell deathNF-E2-Related Factor 2Glucose-regulated proteinApoptosismedicine.disease_causeArticleCatalysisInorganic Chemistrylcsh:ChemistrySettore BIO/10 - BiochimicaAutophagyTumor Cells CulturedmedicineHumansGene silencingoxidative stressPhysical and Theoretical ChemistryEndoplasmic Reticulum Chaperone BiPMolecular Biologylcsh:QH301-705.5tributyltin (IV) derivativeSpectroscopyCell Proliferationoxidative strebiologyChemistryEndoplasmic reticulumOrganic ChemistryAutophagyCancerROSGeneral Medicineendoplasmic reticulum stremedicine.diseaseComputer Science ApplicationsGene Expression Regulation Neoplasticlcsh:Biology (General)lcsh:QD1-999autophagic cell deathColonic NeoplasmsUnfolded protein responseCancer researchbiology.proteinendoplasmic reticulum stressTrialkyltin CompoundsReactive Oxygen SpeciesOxidative stress
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Absence of correlation between oxysterol accumulation in lipid raft microdomains, calcium increase, and apoptosis induction on 158N murine oligodendr…

2013

There is some evidence that oxidized derivatives of cholesterol, 7-ketocholesterol (7KC) and 7β-hydroxycholesterol (7βOHC), are increased in the plasma of patients with neurodegenerative diseases associated with demyelinization of the central nervous system (CNS). It was therefore of interest to investigate the effects of these oxysterols on oligodendrocytes, the myelin-forming cells in the CNS. To this end, 158N murine oligodendrocytes were treated with 7KC or 7βOHC inducing an apoptotic mode of cell death characterized by condensation/fragmentation of the nuclei, dephosphorylation of Akt and GSK3, mitochondrial depolarization involving Mcl-1, and caspase-3 activation. In contrast, under t…

Programmed cell deathOxysterolCell Survivalalpha-TocopherolApoptosisBiologyBiochemistryCell Linechemistry.chemical_compoundGlycogen Synthase Kinase 3MiceMembrane MicrodomainsAnimalsFragmentation (cell biology)Protein kinase BLipid raftKetocholesterolsCell ProliferationPharmacologyDepolarizationHydroxycholesterolsCell biologyOligodendrogliaSterolschemistryProto-Oncogene Proteins c-bcl-2ApoptosisIonomycinMyeloid Cell Leukemia Sequence 1 Proteinlipids (amino acids peptides and proteins)CalciumProto-Oncogene Proteins c-aktBiochemical pharmacology
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Hepatocyte-specific deletion of the antiapoptotic protein myeloid cell leukemia-1 triggers proliferation and hepatocarcinogenesis in mice

2010

Regulation of hepatocellular apoptosis is crucial for liver homeostasis. Increased sensitivity of hepatocytes toward apoptosis results in chronic liver injury, whereas apoptosis resistance is linked to hepatocarcinogenesis and nonresponsiveness to therapy-induced cell death. Recently, we have demonstrated an essential role of the antiapoptotic Bcl-2 family member Myeloid cell leukemia-1 (Mcl-1) in hepatocyte survival. In mice lacking Mcl-1 specifically in hepatocytes (Mcl-1Δhep), spontaneous apoptosis caused severe liver damage. Here, we demonstrate that chronically increased apoptosis of hepatocytes coincides with strong hepatocyte proliferation resulting in hepatocellular carcinoma (HCC).…

Programmed cell deathPathologymedicine.medical_specialty10208 Institute of NeuropathologyApoptosis610 Medicine & health10071 Functional Genomics Center ZurichBiologyArticleMiceLiver Neoplasms Experimental10049 Institute of Pathology and Molecular PathologySurvivinmedicineAnimalsneoplasmsCell ProliferationChromosome AberrationsMice KnockoutHepatologyCell growthLiver cellmedicine.diseaseMyeloid Cell Leukemia Sequence 1 ProteinLeukemiamedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2ApoptosisHepatocyteHepatocytesCancer researchMyeloid Cell Leukemia Sequence 1 Protein570 Life sciences; biology2721 HepatologyU7 Systems Biology / Functional GenomicsHepatology
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Cytotoxicity of apigenin toward multiple myeloma cell lines and suppression of iNOS and COX-2 expression in STAT1-transfected HEK293 cells.

2020

Apigenin is one of the most abundant dietary flavonoids that possesses multiple bio-functions.This study was designed to determine the influence of apigenin on gene expressions, cancer cells, as well as STAT1/COX-2/iNOS pathway mediated inflammation and tumorigenesis in HEK293-STAT1 cells. Furthermore, the cytotoxic activity toward multiple myeloma (MM) cell lines was investigated.Bioinformatic analyses were used to predict the sensitivity and resistance of tumor cells toward apigenin and to determine cellular pathways influenced by this compound. The cytotoxic and ferroptotic activity of apigenin was examined by the resazurin reduction assay. Additionally, we evaluated apoptosis, and cell …

Programmed cell deathPharmaceutical ScienceNitric Oxide Synthase Type IIApoptosis03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCell Line TumorDrug DiscoveryAntineoplastic Combined Chemotherapy ProtocolsAutophagyCytotoxic T cellHumansDAPIApigenin030304 developmental biologyCell ProliferationPharmacology0303 health sciencesDose-Response Relationship DrugChemistryCell CycleComputational BiologyCell cycleAntineoplastic Agents PhytogenicHEK293 CellsSTAT1 Transcription FactorComplementary and alternative medicineApoptosisCell cultureCyclooxygenase 2Doxorubicin030220 oncology & carcinogenesisApigeninCancer cellCancer researchMolecular MedicineMultiple MyelomaReactive Oxygen SpeciesPhytomedicine : international journal of phytotherapy and phytopharmacology
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Pyrazolo[3,4-h]quinolines promising photosensitizing agents in the treatment of cancer.

2015

A new series of pyrazolo[3,4-h]quinolines, heteroanalogues of angelicin was conveniently prepared with a broad substitution pattern. A large number of derivatives was obtained and the cellular photocytotoxicity was evaluated in vitro against 5 different human tumor cell lines with GI50 values reaching the nanomolar level (14.52e0.04 mM). Selected compounds were able to photoinduce a massive cell death with the involvement of mitochondria. Their photodamage cellular targets were proteins and lipids and they did not cause any kind of DNA photodamage. This latter event is of considerable importance in the modulation of long term side effects, generally associated with the use of classical furo…

Programmed cell deathPhotodynamic therapy; Antiproliferative activity; Photosensitizing agents; Reactive oxygen species; PUVA therapyPUVA therapymedicine.medical_treatmentPhotodynamic therapyAntineoplastic AgentsAntiproliferative activityPhotodynamic therapy Antiproliferative activity Photosensitizing agents Reactive oxygen species PUVA therapyMitochondrionPhotodynamic therapychemistry.chemical_compoundStructure-Activity RelationshipAngelicinCell Line TumorDrug DiscoverymedicineStructure–activity relationshipHumansCell ProliferationPharmacologyPhotosensitizing AgentsDose-Response Relationship DrugMolecular StructureCell growthOrganic ChemistryGeneral MedicinePhotosensitizing AgentSettore CHIM/08 - Chimica FarmaceuticaFurocoumarinsBiochemistrychemistryQuinolinesPyrazolesDrug Screening Assays AntitumorReactive oxygen speciesEuropean journal of medicinal chemistry
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Combined inhibition of Bcl-2 and NFκB synergistically induces cell death in cutaneous T-cell lymphoma.

2019

Abstract Therapeutic options for cutaneous T-cell lymphoma (CTCL) are limited and curative treatment regimens are not available. Thus, new targeted and well-tolerated therapeutic approaches are urgently needed. In this respect, we have recently shown that dimethyl fumerate (DMF) inhibits NF-κB acting as a survival factor in CTCL. Similarly, inhibition of the antiapoptotic protein B-cell lymphoma 2 (Bcl-2) has been shown to induce cell death in CTCL especially when combined with histone deacetylase inhibitors. Therefore, we hypothesized that inhibition of Bcl-2 should potentiate NF-κB inhibition in a novel combination treatment of CTCL. We show that, in vitro, the Bcl-2 inhibitors ABT-199 an…

Programmed cell deathT cellImmunologyAntineoplastic AgentsApoptosisBiochemistryMicehemic and lymphatic diseasesCell Line TumormedicineAnimalsHumansRNA Small InterferingCell ProliferationNeoplasm StagingCell DeathDose-Response Relationship Drugbusiness.industryCutaneous T-cell lymphomaNF-kappa BDrug SynergismCell BiologyHematologymedicine.diseaseXenograft Model Antitumor AssaysLymphomaLymphoma T-Cell CutaneousHistone Deacetylase InhibitorsDisease Models Animalmedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2ApoptosisCell cultureCancer researchRNA InterferenceHistone deacetylaseSignal transductionbusinessProtein BindingBlood
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α-Tocopherol impairs 7-ketocholesterol-induced caspase-3-dependent apoptosis involving GSK-3 activation and Mcl-1 degradation on 158N murine oligoden…

2011

Abstract In important and severe neurodegenerative pathologies, 7-ketocholesterol, mainly resulting from cholesterol autoxidation, may contribute to dys- or demyelination processes. On various cell types, 7-ketocholesterol has often been shown to induce a complex mode of cell death by apoptosis associated with phospholipidosis. On 158N murine oligodendrocytes treated with 7-ketocholesterol (20 μg/mL corresponding to 50 μM, 24–48 h), the induction of a mode of cell death by apoptosis characterised by the occurrence of cells with condensed and/or fragmented nuclei, caspase activation (including caspase-3) and internucleosomal DNA fragmentation was observed. It was associated with a loss of tr…

Programmed cell deathTime FactorsCell Survivalalpha-TocopherolApoptosisCaspase 3BiochemistryDephosphorylationGlycogen Synthase Kinase 3MiceMembrane MicrodomainsGSK-3AnimalsKetocholesterolsMolecular BiologyProtein kinase BCell ProliferationMembrane Potential MitochondrialPhospholipidosisGlycogen Synthase Kinase 3 betaCaspase 3ChemistryOrganic ChemistryCytochromes cCell BiologyCell biologyEnzyme ActivationOligodendrogliaProtein TransportProto-Oncogene Proteins c-bcl-2ApoptosisMyeloid Cell Leukemia Sequence 1 ProteinDNA fragmentationChemistry and Physics of Lipids
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