Search results for "Mito"

showing 10 items of 2513 documents

Oxidative stress preconditioning of mouse perivascular myogenic progenitors selects a subpopulation of cells with a distinct survival advantage in vi…

2018

AbstractCell engraftment, survival and integration during transplantation procedures represent the crux of cell-based therapies. Thus, there have been many studies focused on improving cell viability upon implantation. We used severe oxidative stress to select for a mouse mesoangioblast subpopulation in vitro and found that this subpopulation retained self-renewal and myogenic differentiation capacities while notably enhancing cell survival, proliferation and migration relative to unselected cells. Additionally, this subpopulation of cells presented different resistance and recovery properties upon oxidative stress treatment, demonstrating select advantages over parental mesoangioblasts in …

0301 basic medicineCancer ResearchCellular differentiationCellstem cells; oxidative stress; clone isolation/dk/atira/pure/subjectarea/asjc/2800/2804Mice SCIDp38 Mitogen-Activated Protein KinasesMiceCell MovementProtein IsoformsMuscular Dystrophy/dk/atira/pure/subjectarea/asjc/2400/2403Settore BIO/06 - Anatomia Comparata E Citologiaeducation.field_of_studylcsh:CytologyStem CellsSettore BIO/13Cell DifferentiationSkeletalCell biologymedicine.anatomical_structureMuscleMatrix Metalloproteinase 2Animals; Cell Cycle Checkpoints; Cell Differentiation; Cell Line; Cell Movement; Cell Survival; Hydrogen Peroxide; Matrix Metalloproteinase 2; Mice; Mice SCID; Muscle Skeletal; Muscular Dystrophy Animal; Oxidative Stress; Protein Isoforms; Reactive Oxygen Species; Sarcoglycans; Stem Cell Transplantation; Stem Cells; p38 Mitogen-Activated Protein Kinases/dk/atira/pure/subjectarea/asjc/1300/1306/dk/atira/pure/subjectarea/asjc/1300/1307Cell SurvivalPopulationImmunologyBiologySCIDArticleCell Line03 medical and health sciencesCellular and Molecular NeuroscienceIn vivoSarcoglycansmedicineAnimalsProgenitor celllcsh:QH573-671educationMuscle Skeletaloxidative streMesoangioblastAnimalCell BiologyCell Cycle CheckpointsHydrogen PeroxideMuscular Dystrophy Animalclone isolationTransplantationstem cellOxidative Stress030104 developmental biologyCell cultureReactive Oxygen SpeciesStem Cell TransplantationCell Death & Disease
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PHD3 Controls Lung Cancer Metastasis and Resistance to EGFR Inhibitors through TGFα.

2018

Abstract Lung cancer is the leading cause of cancer-related death worldwide, in large part due to its high propensity to metastasize and to develop therapy resistance. Adaptive responses to hypoxia and epithelial–mesenchymal transition (EMT) are linked to tumor metastasis and drug resistance, but little is known about how oxygen sensing and EMT intersect to control these hallmarks of cancer. Here, we show that the oxygen sensor PHD3 links hypoxic signaling and EMT regulation in the lung tumor microenvironment. PHD3 was repressed by signals that induce EMT and acted as a negative regulator of EMT, metastasis, and therapeutic resistance. PHD3 depletion in tumors, which can be caused by the EM…

0301 basic medicineCancer ResearchEpithelial-Mesenchymal TransitionLung NeoplasmsMice NudeAntineoplastic AgentsSMADDrug resistanceMetastasisHypoxia-Inducible Factor-Proline DioxygenasesMitochondrial Proteins03 medical and health sciencesErlotinib HydrochlorideMice0302 clinical medicineDownregulation and upregulationCell Line TumorTumor MicroenvironmentMedicineAnimalsHumansNeoplasm MetastasisLung cancerProtein Kinase InhibitorsEGFR inhibitorsbusiness.industryIntracellular Signaling Peptides and ProteinsCancerTransforming Growth Factor alphamedicine.diseaseHCT116 CellsXenograft Model Antitumor AssaysCell HypoxiaErbB Receptors030104 developmental biologyOncologyA549 CellsDrug Resistance Neoplasm030220 oncology & carcinogenesisembryonic structuresCancer researchFemaleErlotinibbusinessApoptosis Regulatory Proteinsmedicine.drugCancer research
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Doxorubicin anti-tumor mechanisms include Hsp60 post-translational modifications leading to the Hsp60/p53 complex dissociation and instauration of re…

2017

Hsp60 is a pro-carcinogenic chaperonin in certain tumor types by interfering with apoptosis and with tumor cell death. In these tumors, it is not known whether or not doxorubicin anti-tumor effects include a blockage of the pro-carcinogenic action of this protein. We used the human lung mucoepidermoid cell line NCI-H292 and different doses of doxorubicin to measure cell viability, cell cycle progression, cell senescence indicators, Hsp60 levels and its post-translational modifications as well as the release of the chaperonin into the extracellular environment. Cell viability was reduced in relation to doxorubicin dose and this was paralleled by the appearance of cell senescence markers. Con…

0301 basic medicineCancer ResearchLung NeoplasmsChaperoninsCellApoptosismedicine.disease_causeHistones0302 clinical medicineCellular SenescenceAntibiotics AntineoplasticAcetylationG2 Phase Cell Cycle Checkpointsmedicine.anatomical_structureOncology030220 oncology & carcinogenesisCell agingIntracellularProtein BindingSignal TransductionSenescenceCyclin-Dependent Kinase Inhibitor p21animal structuresCell Survivalchemical and pharmacologic phenomenaBiologycomplex mixturesMitochondrial ProteinsDoxorubicin Hsp60 Acetylation Ubiquitination p53 Replicative senescence03 medical and health sciencesDoxorubicin; Hsp60; p53; replicative senescence; post-translational modificationsCell Line TumormedicineHumansCell Proliferationdoxorubicin p53 Hsp60Dose-Response Relationship DrugCell growthfungiUbiquitinationChaperonin 60Molecular biology030104 developmental biologyAcetylationApoptosisDoxorubicinProteolysisCancer researchCarcinoma MucoepidermoidTumor Suppressor Protein p53CarcinogenesisProtein Processing Post-Translational
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The PDGFRβ/ERK1/2 pathway regulates CDCP1 expression in triple-negative breast cancer

2018

Background CDCP1, a transmembrane protein with tumor pro-metastatic activity, was recently identified as a prognostic marker in TNBC, the most aggressive breast cancer subtype still lacking an effective molecular targeted therapy. The mechanisms driving CDCP1 over-expression are not fully understood, although several stimuli derived from tumor microenvironment, such as factors present in Wound Healing Fluids (WHFs), reportedly increase CDCP1 levels. Methods The expression of CDCP1, PDGFRβ and ERK1/2cell was tested by Western blot after stimulation of MDA-MB-231 cells with PDGF-BB and, similarly, in presence or not of ERK1/2 inhibitor in a panel of TNBC cell lines. Knock-down of PDGFRβ was e…

0301 basic medicineCancer ResearchMAP Kinase Signaling SystemCDCP1medicine.medical_treatmentPDGFRβPDGF-BBBecaplerminTriple Negative Breast NeoplasmsBiologylcsh:RC254-282Targeted therapyReceptor Platelet-Derived Growth Factor beta03 medical and health sciences0302 clinical medicineFISHDownregulation and upregulationWestern blotAntigens CDAntigens NeoplasmCell Line TumorGeneticsmedicineHumansRNA Small InterferingReceptorTriple-negative breast cancerMitogen-Activated Protein Kinase 1Tumor microenvironmentMitogen-Activated Protein Kinase 3ERK1/2medicine.diagnostic_testMiddle Agedlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensNeoplasm ProteinsUp-RegulationGene Expression Regulation Neoplastic030104 developmental biologyOncologyGene Knockdown Techniques030220 oncology & carcinogenesisCDCP1Cancer researchImmunohistochemistryFemaleCell Adhesion MoleculesTNBCResearch ArticleIHCBMC Cancer
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Integrating the Tumor Microenvironment into Cancer Therapy

2020

© 2020 by the authors.

0301 basic medicineCancer ResearchMechanotransductionReviewGut floralcsh:RC254-28203 medical and health sciences0302 clinical medicineImmune systemStromamedicineMechanotransductionStromal reprogrammingTumor microenvironmentbiologybusiness.industryMicrobiotaCancerlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseasebiology.organism_classificationPrognostic toolsMetforminMitochondria030104 developmental biologyMetabolismOncologyImmune therapyTumor progression030220 oncology & carcinogenesisCancer researchBiomarker discoverybusinessReprogrammingVitamin D3
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Parthenolide and DMAPT exert cytotoxic effects on breast cancer stem-like cells by inducing oxidative stress, mitochondrial dysfunction and necrosis

2016

Triple-negative breast cancers (TNBCs) are aggressive forms of breast carcinoma associated with a high rate of recidivism. In this paper, we report the production of mammospheres from three lines of TNBC cells and demonstrate that both parthenolide (PN) and its soluble analog dimethylaminoparthenolide (DMAPT) suppressed this production and induced cytotoxic effects in breast cancer stem-like cells, derived from dissociation of mammospheres. In particular, the drugs exerted a remarkable inhibitory effect on viability of stem-like cells. Such an effect was suppressed by N-acetylcysteine, suggesting a role of reactive oxygen species (ROS) generation in the cytotoxic effect. Instead z-VAD, a ge…

0301 basic medicineCancer ResearchNecrosismedicine.disease_causeCancer -- Treatmentchemistry.chemical_compoundOnium CompoundsMedicineCytotoxic T cellBreast -- CancerMembrane Potential Mitochondrialchemistry.chemical_classificationSuperoxideMitochondrial DNAMitochondriaNeoplastic Stem CellsFemaleOriginal Articlemedicine.symptomOligopeptidesSesquiterpenesCell SurvivalNF-E2-Related Factor 2ImmunologyBreast NeoplasmsReal-Time Polymerase Chain Reaction03 medical and health sciencesCellular and Molecular NeuroscienceDownregulation and upregulationCell Line TumorHumansParthenolideparthenolide cancer stem cell triple-negative breast cancer reactive oxygen species nuclear factor erythroid 2-related factor 2Fluorescent DyesReactive oxygen speciesbusiness.industryAcetophenonesNADPH OxidasesCell BiologyCell nuclei -- AbnormalitiesOxidative Stress030104 developmental biologychemistryApocyninImmunologyCancer researchReactive Oxygen SpeciesbusinessOxidative stressTranscription FactorsCell Death & Disease
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Betulinic acid induces a novel cell death pathway that depends on cardiolipin modification

2016

Cancer is associated with strong changes in lipid metabolism. For instance, normal cells take up fatty acids (FAs) from the circulation, while tumour cells generate their own and become dependent on de novo FA synthesis, which could provide a vulnerability to target tumour cells. Betulinic acid (BetA) is a natural compound that selectively kills tumour cells through an ill-defined mechanism that is independent of BAX and BAK, but depends on mitochondrial permeability transition-pore opening. Here we unravel this pathway and show that BetA inhibits the activity of steroyl-CoA-desaturase (SCD-1). This enzyme is overexpressed in tumour cells and critically important for cells that utilize de n…

0301 basic medicineCancer ResearchProgrammed cell deathCardiolipinsMitochondrionCell Line03 medical and health scienceschemistry.chemical_compoundSDG 3 - Good Health and Well-beingBetulinic acidGeneticsCardiolipinHumansBetulinic AcidCytotoxicityMolecular BiologyCell DeathbiologyCytochrome cFatty AcidsCytochromes cLipid metabolismAntineoplastic Agents PhytogenicTriterpenesMitochondriaCell biology030104 developmental biologyBiochemistrychemistryCancer cellbiology.protein/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_beingPentacyclic TriterpenesStearoyl-CoA Desaturase
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2-Methoxyestradiol Affects Mitochondrial Biogenesis Pathway and Succinate Dehydrogenase Complex Flavoprotein Subunit A in Osteosarcoma Cancer Cells.

2017

Background/aim Dysregulation of mitochondrial pathways is implicated in several diseases, including cancer. Notably, mitochondrial respiration and mitochondrial biogenesis are favored in some invasive cancer cells, such as osteosarcoma. Hence, the aim of the current work was to investigate the effects of 2-methoxyestradiol (2-ME), a potent anticancer agent, on the mitochondrial biogenesis of osteosarcoma cells. Materials and methods Highly metastatic osteosarcoma 143B cells were treated with 2-ME separately or in combination with L-lactate, or with the solvent (non-treated control cells). Protein levels of α-syntrophin and peroxisome proliferator-activated receptor gamma, coactivator 1 alph…

0301 basic medicineCancer ResearchSIRT3Protein subunitSDHAMuscle ProteinsAntineoplastic AgentsMolecular Dynamics SimulationBiochemistryElectron Transport Complex IV03 medical and health sciences0302 clinical medicineGeneticSettore BIO/10 - BiochimicaCell Line TumorSirtuin 3CoactivatorGeneticsHumansMolecular BiologyOsteosarcomaOrganelle BiogenesisbiologyEstradiolSettore BIO/16 - Anatomia UmanaChemistryElectron Transport Complex IICalcium-Binding ProteinsMembrane ProteinsPeroxisomeMitochondrial biogenesiPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaCell biology2-MethoxyestradiolMitochondriaSuccinate dehydrogenaseMolecular Docking Simulation030104 developmental biologyMitochondrial biogenesisSettore CHIM/03 - Chimica Generale E Inorganica030220 oncology & carcinogenesisSirtuinCancer cellbiology.proteinResearch ArticleCancer genomicsproteomics
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Nut1/Hos1 and Sas2/Rpd3 control the H3 acetylation of two different sets of osmotic stress-induced genes

2019

Epigenetic information is able to interact with the cellular environment and could be especially useful for reprograming gene expression in response to a physiological perturbation. In fact the genes induced or repressed by osmotic stress undergo significant changes in terms of the levels of various histone modifications, especially in the acetylation levels of histone H3. Exposing yeast to high osmolarity results in the activation of stress-activated protein kinase Hog1, which plays a central role in gene expression control. We evaluated the connection between the presence of Hog1 and changes in histone H3 acetylation in stress-regulated genes. We found a parallel increase in the acetylati…

0301 basic medicineCancer ResearchSaccharomyces cerevisiae Proteinschip-on-chipSaccharomyces cerevisiaeEpigenesis GeneticHistones03 medical and health sciencesHistone H30302 clinical medicineOsmotic PressureGene Expression Regulation FungalGene expressionEpigeneticsHistone H3 acetylationMolecular BiologyHistone AcetyltransferasesRegulation of gene expressionMediator ComplexbiologyepigeneticsAcetylationCell biologyChromatinDNA-Binding ProteinsHistone Code030104 developmental biologyHistoneHistone acetylationAcetylation030220 oncology & carcinogenesisbiology.proteinchromatinhog1osmotic stressMitogen-Activated Protein Kinasesgene regulationProtein Processing Post-TranslationalTranscription FactorsResearch Paper
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Parthenolide prevents resistance of MDA-MB231 cells to doxorubicin and mitoxantrone: the role of Nrf2.

2017

Triple-negative breast cancer is a group of aggressive cancers with poor prognosis owing to chemoresistance, recurrence and metastasis. New strategies are required that could reduce chemoresistance and increases the effectiveness of chemotherapy. The results presented in this paper, showing that parthenolide (PN) prevents drug resistance in MDA-MB231 cells, represent a contribution to one of these possible strategies. MDA-MB231 cells, the most studied line of TNBC cells, were submitted to selection treatment with mitoxantrone (Mitox) and doxorubicin (DOX). The presence of resistant cells was confirmed through the measurement of the resistance index. Cells submitted to this treatment exhibit…

0301 basic medicineCancer ResearchSmall interfering RNATriple-negative breast cancer resistance parthenolideImmunologyStimulationCancer -- TreatmentArticle03 medical and health sciencesCellular and Molecular Neurosciencechemistry.chemical_compound0302 clinical medicineDownregulation and upregulationSettore BIO/10 - BiochimicamedicineChemotherapyDoxorubicinParthenolideBreast -- CancerDrug resistance in cancer cellsMitoxantroneChemistryCell BiologyTransfectionHsp70030104 developmental biology030220 oncology & carcinogenesisCancer researchmedicine.drugCell death discovery
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