2021
Nucleotide‐binding domain and leucine‐rich‐repeat‐containing protein X1 deficiency induces nicotinamide adenine dinucleotide decline, mechanistic target of rapamycin activation, and cellular senescence and accelerates aging lung‐like changes
Shin HJ, Kim S, Park H, Shin M, Kang I, Kang M. Nucleotide‐binding domain and leucine‐rich‐repeat‐containing protein X1 deficiency induces nicotinamide adenine dinucleotide decline, mechanistic target of rapamycin activation, and cellular senescence and accelerates aging lung‐like changes. Aging Cell 2021, 20: e13410. PMID: 34087956, PMCID: PMC8282248, DOI: 10.1111/acel.13410.Peer-Reviewed Original ResearchConceptsCellular senescenceActivation of mTORNucleotide-binding domainCellular senescence responseReplicative cellular senescenceNLR family membersOrganismal agingCellular physiologyMitochondrial moleculesSenescence responseCellular locationProtein X1Crucial regulatorMechanistic targetMitochondrial functionMolecular hallmarksNLRX1 functionRapamycin (mTOR) activationMitochondrial dysfunctionSenescenceMTORPharmacological inhibitionNLRX1BiologyAging Lung
2018
Salinomycin ameliorates oxidative hepatic damage through AMP-activated protein kinase, facilitating autophagy
Kim K, Lee S, Baek S, Lee E, Jang E, Lee J, Ahn S, Chang J, Oh T, Kim S, Ma J, Kim S, Park K, Kim Y. Salinomycin ameliorates oxidative hepatic damage through AMP-activated protein kinase, facilitating autophagy. Toxicology And Applied Pharmacology 2018, 360: 141-149. PMID: 30290169, DOI: 10.1016/j.taap.2018.10.002.Peer-Reviewed Original ResearchConceptsImportance of AMPKMitochondrial dysfunctionAcidic vesicle organellesOxidative stressProtein kinase activationReactive oxygen species productionProtein kinaseAMPK inhibitionKinase activationSevere oxidative stressOxygen species productionLiver injuryMolecular mechanismsIron-induced apoptosisHepatic protectantStreptomyces albusHuman diseasesAMPKCellular mechanismsLC3-IISalinomycin's effectsArachidonic acidMitochondrial impairmentROS productionAnti-cancer agents
2017
Salinomycin Induces Reactive Oxygen Species and Apoptosis in Aggressive Breast Cancer Cells as Mediated with Regulation of Autophagy
Kim K, Park K, Kim S, Yu S, Lee D, Kim Y, Noh K, YEUL J, Seo Y, Ahn S. Salinomycin Induces Reactive Oxygen Species and Apoptosis in Aggressive Breast Cancer Cells as Mediated with Regulation of Autophagy. Anticancer Research 2017, 37: 1747-1758. PMID: 28373437, DOI: 10.21873/anticanres.11507.Peer-Reviewed Original ResearchConceptsMDA-MB-231 cellsAggressive breast cancer cellsBreast cancer cellsCancer cellsReactive oxygen speciesBreast cancer cell linesROS productionMitochondrial membrane potentialScavenger of ROSInduces reactive oxygen speciesCancer cell linesCaspase-3/9 activityPropidium iodide stainingMCF-7 cellsOxygen speciesAcceleration of apoptosisAcridine orange stainingAutophagy inhibitionMonocarboxylic ionophoreChemotherapeutic drugsCancer treatmentMitochondrial dysfunctionIodide stainingRegulation of autophagyUnderlying mechanism
2016
Toyocamycin induces apoptosis via the crosstalk between reactive oxygen species and p38/ERK MAPKs signaling pathway in human prostate cancer PC-3 cells
Park S, Kim S, Kim K, Yu S, Choi H, Kim Y, Nam H, Seo Y, Ahn S. Toyocamycin induces apoptosis via the crosstalk between reactive oxygen species and p38/ERK MAPKs signaling pathway in human prostate cancer PC-3 cells. Pharmacological Reports 2016, 69: 90-96. PMID: 27912102, DOI: 10.1016/j.pharep.2016.10.014.Peer-Reviewed Original ResearchConceptsProstate cancer PC-3 cellsPC-3 cellsCancer PC-3 cellsOxygen species productionROS productionERK MAPKNon-malignant RWPE-1 cellsExtracellular signal-regulated kinase (ERK) activityMitochondrial dysfunctionSpecies productionMitochondrial membrane potentialCell cycle arrestHuman prostate cancer PC-3 cellsReactive oxygen species productionCell viabilityRWPE-1 cellsProtein kinaseStreptomyces speciesKinase activityReactive oxygen speciesERK activationMolecular mechanismsP38 activationMAPK proteinsApoptotic effects