Search results for "endoplasmic reticulum stre"

showing 10 items of 52 documents

Cellular stress induces cap-independent alpha-enolase/MBP-1 translation.

2015

AbstractMyc promoter-binding protein-1 (MBP-1) is a shorter protein variant of the glycolytic enzyme alpha-enolase. Although several lines of evidence indicate that MBP-1 acts as a tumor suppressor, the cellular mechanisms and signaling pathways underlying MBP-1 expression still remain largely elusive. To dissect these pathways, we used the SkBr3 breast cancer cell line and non-tumorigenic HEK293T cells ectopically overexpressing alpha-enolase/MBP-1. Here, we demonstrate that induced cell stresses promote MBP-1 expression through the AKT/PERK/eIF2α signaling axis. Our results contribute to shedding light on the molecular mechanisms underlying MBP-1 expression in non-tumorigenic and cancer c…

Alpha-enolaseCellEukaryotic Initiation Factor-2Alternative translationBiochemistryeIF-2 KinaseBreast cancerHEK293 CellStructural BiologyProtein IsoformsbiologyMedicine (all)Translation (biology)Recombinant ProteinEndoplasmic Reticulum StressRecombinant ProteinsNeoplasm ProteinsDNA-Binding ProteinsGene Expression Regulation Neoplasticmedicine.anatomical_structureFemaleSignal transductionMyc promoter-binding protein-1Breast NeoplasmHumanSignal TransductionCell SurvivalDNA-Binding ProteinRecombinant Fusion ProteinsBiophysicsBreast NeoplasmsNeoplasm ProteinGeneticCell Line TumorEndoplasmic reticulum streGeneticsmedicineBiomarkers TumorHumansGene SilencingMolecular BiologyProtein kinase BTumor Suppressor ProteinTumor Suppressor ProteinsHEK 293 cellsProtein IsoformCell BiologySettore BIO/18 - GeneticaHEK293 CellsBiophysicGene Expression RegulationPhosphopyruvate HydrataseCancer cellbiology.proteinUnfolded protein responseCancer researchProto-Oncogene Proteins c-aktRecombinant Fusion ProteinFEBS letters
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Does Metformin Modulate Endoplasmic Reticulum Stress and Autophagy in Type 2 Diabetic Peripheral Blood Mononuclear Cells?

2018

Since type 2 diabetes (T2D) is associated with oxidative stress and metformin has been shown to exert a protective role against the said stress, we wondered whether metformin treatment might also modulate endoplasmic reticulum (ER) stress and autophagy in leukocytes of T2D patients. We studied 53 T2D patients (37 of whom had been treated with metformin 1700 mg for at least 1 year) and 30 healthy volunteers. Leukocytes from both groups of T2D patients exhibited increased protein levels of 78-kDa glucose-regulated protein (GRP78) with respect to controls, whereas activating transcription factor 6 (ATF6) was enhanced specifically in nonmetformin-treated T2D, and (s-xbp1) and phosphorylated euk…

Male0301 basic medicinemedicine.medical_specialtyendocrine system diseasesPhysiologyClinical BiochemistryAdministration OralType 2 diabetesBiologymedicine.disease_causeBiochemistry03 medical and health sciencesInternal medicineAutophagymedicineHumansEndoplasmic Reticulum Chaperone BiPMolecular BiologyGeneral Environmental ScienceDose-Response Relationship DrugATF6Endoplasmic reticulumAutophagynutritional and metabolic diseasesCell BiologyBECN1Middle AgedEndoplasmic Reticulum Stressmedicine.diseaseMetforminMetforminOxidative StressCross-Sectional Studies030104 developmental biologyEndocrinologyDiabetes Mellitus Type 2Leukocytes MononuclearUnfolded protein responseGeneral Earth and Planetary SciencesFemaleOxidative stressmedicine.drugAntioxidants & Redox Signaling
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Endoplasmic reticulum stress is involved in response of human laryngeal carcinoma cells to carboplatin but is absent in carboplatin resistant cells

2013

The major obstacle of successful tumor treatment with carboplatin (CBP) is the development of drug resistance. In the present study, we found that following treatment with CBP the amount of platinum which enters the human laryngeal carcinoma (HEp2)-derived CBP- resistant (7T) cells is reduced relative to the parental HEp2. As a consequence, the formation of reactive oxidative species (ROS) is reduced, the induction of endoplasmic reticulum (ER) stress is diminished, the amount of inter- and intrastrand cross-links is lower, and the induction of apoptosis is depressed. In HEp2 cells, ROS scavenger tempol, inhibitor of ER stress salubrinal, as well as gene silencing of ER stress marker CCAAT/…

Celllcsh:MedicineApoptosisCarboplatinSalubrinalapoptosis; carboplatin; drug resistance; endoplasmic reticulum stress; reactive oxidative species; tumor cellschemistry.chemical_compound0302 clinical medicineBlotting Southwesternlcsh:Science0303 health sciencesMultidisciplinaryThioureaGeologyEndoplasmic Reticulum Stress3. Good healthmedicine.anatomical_structure030220 oncology & carcinogenesisSignal transductionSignal TransductionResearch ArticleProgrammed cell deathCell SurvivalBlotting WesternBiologyReal-Time Polymerase Chain ReactionCyclic N-Oxides03 medical and health sciencesCell Line TumormedicineHumansGene SilencingLaryngeal NeoplasmsBiology030304 developmental biologyDNA PrimersPlatinumEndoplasmic reticulumlcsh:RCarcinomaMolecular biologychemistryCell cultureApoptosisCinnamatesDrug Resistance NeoplasmUnfolded protein responseCancer researchlcsh:QSpin LabelsReactive Oxygen Species
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Normalization of sphingomyelin levels by 2-hydroxyoleic acid induces autophagic cell death of SF767 cancer cells

2012

The very high mortality rate of gliomas reflects the unmet therapeutic need associated with this type of brain tumor. We have discovered that the plasma membrane fulfills a critical role in the propagation of tumorigenic signals, whereby changes in membrane lipid content can either activate or silence relevant pathways. We have designed a synthetic fatty acid, 2-hydroxyoleic acid (2OHOA), that specifically activates sphingomyelin synthase (SGMS), thereby modifying the lipid content of cancer cell membranes and restoring lipid levels to those found in normal cells. In reverting, the structure of the membrane by activating SGMS, 2OHOA inhibits the RAS-MAPK pathway, which in turn fails to acti…

Programmed cell deathCellular differentiationOleic AcidsBiologyModels BiologicalCell membrane2-Hydroxyoleic AcidCell Line TumorSphingomyelin synthaseAutophagymedicineHumanscancerMolecular BiologyphospholipidCell CycleGliomaCell Biologylipid bilayer and proliferationCell cycleEndoplasmic Reticulum StressAutophagic PunctumSphingomyelinsCell biologyminervalmedicine.anatomical_structureCancer cellbiology.proteinsignalingSphingomyelincell membraneSignal TransductionAutophagy
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Role of Endoplasmic Reticulum and Oxidative Stress Parameters in the Pathophysiology of Disease-Related Malnutrition in Leukocytes of an Outpatient P…

2019

Cellular pathways such as inflammation or oxidative stress are the cause and triggers of disease-related malnutrition (DRM), but the influence of these markers on endoplasmic reticulum (ER) stress is unknown. The objective of this study was to analyze the relationship between mitochondrial function and ER stress parameters in a DRM population. The study population was composed of 82 outpatient subjects, of whom 45 were diagnosed with DRM and 37 were confirmed to be normonourished according to the American Society for Parenteral and Enteral Nutrition ASPEN criteria. We evaluated anthropometrical and biochemical parameters, pro-inflammatory cytokines in serum. Oxidative and ER stress markers …

AdultMale0301 basic medicinemedicine.medical_specialtyPopulationNutritional Statuslcsh:TX341-641InflammationOxidative phosphorylationEndoplasmic Reticulummedicine.disease_cause03 medical and health sciences0302 clinical medicinemitochondrial functionInternal medicineOutpatientsdisease-related malnutritionLeukocytesmedicineHumans030212 general & internal medicineeducationoutpatient populationAgededucation.field_of_study030109 nutrition & dieteticsNutrition and DieteticsAnthropometryATF6business.industryBrief ReportEndoplasmic reticulumMalnutritionMiddle AgedOxidative StressEndocrinologyinflammationendoplasmic reticulum stressUnfolded protein responseCytokinesFemaleSignal transductionmedicine.symptombusinesslcsh:Nutrition. Foods and food supplyOxidative stressFood ScienceNutrients
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Impact of polymer-modified gold nanoparticles on brain endothelial cells: exclusion of endoplasmic reticulum stress as a potential risk factor

2016

A library of polymer-coated gold nanoparticles (AuNPs) differing in size and surface modifications was examined for uptake and induction of cellular stress responses in the endoplasmic reticulum (ER stress) in human brain endothelial cells (hCMEC/D3). ER stress is known to affect the physiology of endothelial cells (ECs) and may lead to inflammation or apoptosis. Thus, even if applied at non-cytotoxic concentrations ER stress caused by nanoparticles should be prevented to reduce the risk of vascular diseases and negative effects on the integrity of barriers (e.g. blood-brain barrier). We exposed hCMEC/D3 to twelve different AuNPs (three sizes: 18, 35, and 65 nm, each with four surface-modif…

0301 basic medicineXBP1BiPCell SurvivalPolymersBiomedical EngineeringMetal NanoparticlesApoptosis02 engineering and technologyBiologyEndoplasmic ReticulumToxicologyArticleCell LineProinflammatory cytokine03 medical and health sciencescell stressDownregulation and upregulationRisk FactorsHeat shock proteinAnimalsHumansHSP70 Heat-Shock ProteinsParticle SizeHeat-Shock ProteinsATF6Endoplasmic reticulumInterleukin-8ATF4Endothelial CellsMembrane Proteinsunfolded protein responseEndoplasmic Reticulum Stress021001 nanoscience & nanotechnologyQPActivating Transcription Factor 4Cell biology030104 developmental biologyBlood-Brain Barriertight junction proteinsImmunologyUnfolded protein responseGold0210 nano-technologyTranscription Factor CHOPNanotoxicology
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Moderate weight loss attenuates chronic endoplasmic reticulum stress and mitochondrial dysfunction in human obesity

2018

Abstract Objective In obese patients undergoing caloric restriction, there are several potential mechanisms involved in the improvement of metabolic outcomes. The present study further explores whether caloric restriction can modulate endoplasmic reticulum (ER) stress and mitochondrial function, as both are known to be mechanisms underlying inflammation and insulin resistance (IR) during obesity. Methods A total of 64 obese patients with BMI ≥35 kg/m2 underwent a dietary program consisting of 6 weeks of a very-low-calorie diet followed by 18 weeks of low-calorie diet. We evaluated changes in the metabolic and inflammatory markers -TNFα, hsCRP, complement component 3 (C3c), and retinol bindi…

Male0301 basic medicineGPX1MitochondrionSystemic inflammationmedicine.disease_causeGlutathione Peroxidase GPX10302 clinical medicineSirtuin 1Endoplasmic Reticulum Chaperone BiPHeat-Shock ProteinsMembrane Potential MitochondrialbiologyComplement C3Middle AgedEndoplasmic Reticulum StressMitochondriaC-Reactive ProteinFemalemedicine.symptomAdultmedicine.medical_specialty030209 endocrinology & metabolism03 medical and health sciencesInsulin resistanceInternal medicineWeight LossmedicineHumansObesityMolecular BiologyCaloric RestrictionInflammationGlutathione PeroxidaseRetinol binding protein 4Tumor Necrosis Factor-alphabusiness.industryEndoplasmic reticulumCell Biologymedicine.disease030104 developmental biologyEndocrinologySpainbiology.proteinUnfolded protein responseInsulin ResistanceReactive Oxygen SpeciesbusinessRetinol-Binding Proteins PlasmaOxidative stressMolecular Metabolism
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Targeting COPZ1 non-oncogene addiction counteracts the viability of thyroid tumor cells

2017

Abstract Thyroid carcinoma is generally associated with good prognosis, but no effective treatments are currently available for aggressive forms not cured by standard therapy. To find novel therapeutic targets for this tumor type, we had previously performed a siRNA-based functional screening to identify genes essential for sustaining the oncogenic phenotype of thyroid tumor cells, but not required to the same extent for the viability of normal cells (non-oncogene addiction paradigm). Among those, we found the coatomer protein complex ζ1 (COPZ1) gene, which is involved in intracellular traffic, autophagy and lipid homeostasis. In this paper, we investigated the mechanisms through which COPZ…

0301 basic medicineCancer ResearchTime FactorsCOPZ1ApoptosisCOPZ1Thyroid cancerThyroid NeoplasmThyroidRNAi TherapeuticCell death; COPZ1; Non-oncogene addiction; Thyroid carcinoma; Animals; Apoptosis; Autophagy; Cell Line Tumor; Cell Survival; Coatomer Protein; Endoplasmic Reticulum Stress; Female; Gene Expression Regulation Neoplastic; Humans; Mice Nude; RNA Interference; Signal Transduction; Thyroid Neoplasms; Time Factors; Transfection; Tumor Burden; Unfolded Protein Response; Xenograft Model Antitumor Assays; RNAi Therapeutics; Oncology; Cancer ResearchEndoplasmic Reticulum StressOncogene AddictionTumor BurdenGene Expression Regulation Neoplasticmedicine.anatomical_structureOncologyFemaleRNA InterferenceNon-oncogene addictionHumanSignal TransductionCell deathProgrammed cell deathXenograft Model Antitumor AssayTime FactorCell SurvivalMice NudeBiologyTransfectionCoatomer ProteinThyroid carcinomaThyroid carcinoma03 medical and health sciencesCell Line TumorAutophagymedicineAnimalsHumansThyroid NeoplasmsEndoplasmic Reticulum StreAnimalAutophagyApoptosimedicine.diseaseXenograft Model Antitumor AssaysRNAi Therapeutics030104 developmental biologyImmunologyUnfolded Protein ResponseCancer researchUnfolded protein response
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Homocysteine Induces Apoptosis of Human Umbilical Vein Endothelial Cells via Mitochondrial Dysfunction and Endoplasmic Reticulum Stress

2017

Homocysteine- (Hcy-) induced endothelial cell apoptosis has been suggested as a cause of Hcy-dependent vascular injury, while the proposed molecular pathways underlying this process are unclear. In this study, we investigated the adverse effects of Hcy on human umbilical vein endothelial cells (HUVEC) and the underlying mechanisms. Our results demonstrated that moderate-dose Hcy treatment induced HUVEC apoptosis in a time-dependent manner. Furthermore, prolonged Hcy treatment increased the expression of NOX4 and the production of intracellular ROS but decreased the ratio of Bcl-2/Bax and mitochondrial membrane potential (MMP), resulting in the leakage of cytochrome c and activation of caspa…

0301 basic medicineAgingArticle SubjectApoptosis030204 cardiovascular system & hematologyTransfectionBiochemistryUmbilical vein03 medical and health sciences0302 clinical medicineRisk FactorsHuman Umbilical Vein Endothelial CellsHumanslcsh:QH573-671Protein kinase AEndoplasmic Reticulum Chaperone BiPHomocysteinebiologylcsh:CytologyKinaseEndoplasmic reticulumCytochrome cCell BiologyGeneral MedicineEndoplasmic Reticulum StressMitochondriaCell biology030104 developmental biologyApoptosiscardiovascular systemUnfolded protein responsebiology.proteinPhosphorylationResearch ArticleOxidative Medicine and Cellular Longevity
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Mitochondria and T2D: Role of Autophagy, ER Stress, and Inflammasome

2020

Type 2 diabetes (T2D) is one of the main current threats to human health. Both T2D and its numerous clinical complications are related to mitochondrial dysfunction and oxidative stress. Over the past decade, great progress has been made in extending our knowledge about the signaling events regulated by mitochondria. However, the links among mitochondrial impairment, oxidative stress, autophagy, endoplasmic reticulum (ER) stress, and activation of the inflammasome still need to be clarified. In light of this deficit, we aim to provide a review of the existing literature concerning the complicated crosstalk between mitochondrial impairment, autophagy, ER stress, and the inflammasome in the mo…

Oxidative stressAutophagyEndoplasmic reticulum stressType 2 diabetesInflammasomeMitochondria
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