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Salinomycin induces endoplasmic reticulum stressmediated autophagy and apoptosis through generation of reactive oxygen species in human glioma U87MG cells

Authors
Yu, SN; Kim, SH; Kim, KY; Ji, JH; Seo, YK; Yu, HS; Ahn, SC
Citation
Oncology reports, 37(6):3321-3328, 2017
Journal Title
Oncology reports
ISSN
1021-335X1791-2431
Abstract
Salinomycin is a polyether ionophore antibiotic that has recently been shown to induce cell apoptosis in human cancer cells displaying multiple mechanisms of drug resistance. In the present study, we explored the impact of salinomycin on the apoptosis and autophagy as well as the correlation between those effects and endoplasmic reticulum (ER) stress molecular mechanisms in human glioma U87MG cells. Apoptosis, autophagy and reactive oxygen species (ROS) were analyzed using flow cytometry. In addition, expression levels of apoptosis-, autophagy- and ER stress-related proteins were determined by western blotting. The results showed that salinomycin induced apoptosis, ER stress and autophagy in glioma cancer cell lines. In addition, salinomycin also induced ROS generation, and the ROS scavenger N-acetyl-L-cysteine was found to inhibit the salinomycin-induced apoptosis, ER stress and autophagy. The inhibition of ER stress with 4-phenylbutyric acid depressed salinomycin-induced apoptosis and autophagy. Salinomycin increased the expression of autophagy marker protein, LC3B, and accumulation of acidic vesicular organelles. Furthermore, pre-treatment with the autophagy inhibitor 3-methyladenine showed potential in increasing the apoptosis rate induced by salinomycin in the U87MG cells. Taken together, these results revealed that salinomycin induced apoptosis and autophagy via ER stress mediated by ROS, suggesting that ER stress by salinomycin plays a dual function in both promoting and suppressing cell death.
MeSH terms
Apoptosis/drug effectsAutophagy/drug effects*Cell Line, TumorCell Proliferation/drug effects*Endoplasmic Reticulum/drug effectsEndoplasmic Reticulum Stress/drug effectsGlioma/drug therapy*Glioma/geneticsGlioma/pathologyHumansPyrans/administration & dosage*Reactive Oxygen Species/metabolism
DOI
10.3892/or.2017.5615
PMID
28498472
Appears in Collections:
Journal Papers > Research Organization > Genomic Instability Research Center
AJOU Authors
지, 재훈
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