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Salinomycin simultaneously induces apoptosis and autophagy through generation of reactive oxygen species in osteosarcoma U2OS cells

Author(s)
Kim, Sang-HunChoi, Young-JunKim, Kwang-YounYu, Sun-NyoungSeo, Young KyoChun, Sung-SikNoh, Kyung-TaeSuh, Jeung-TakAhn, Soon-Cheol
Issued Date
2016-04
DOI
10.1016/j.bbrc.2016.03.132
URI
https://scholarworks.unist.ac.kr/handle/201301/18967
Fulltext
http://www.sciencedirect.com/science/article/pii/S0006291X16304442
Citation
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.473, no.2, pp.607 - 613
Abstract
Salinomycin, a polyether antibiotic, acts as a highly selective potassium ionophore. It was reported to anticancer activity on various cancer cell lines. In this study, salinomycin was examined on apoptosis and autophagy through generation of reactive oxygen species (ROS) in osteosarcoma U2OS cells. Apoptosis, autophagy, mitochondrial membrane potential (MMP) and ROS were analyzed using flow cytometry. Also, expressions of apoptosis- and autophagy-related proteins were determined by western blotting. As a result, salinomycin triggered apoptosis of U2OS cells, which was accompanied by change of MMP and cleavage of caspases-3 and poly (ADP-ribose) polymerase. And salinomycin increased the expression of autophagy-related protein and accumulation of acidic vesicular organelles (AVO). Salinomycin-induced ROS production promotes both apoptosis and autophagy, as evidenced by the result that treatment of N-acetyl-l-cysteine (NAC), a ROS scavenger, attenuated both apoptosis and autophagy. In addition, inhibition of autophagy by 3-methyladenine (3 MA) enhanced the salinoymcin-induced apoptosis. Taken together, these results suggested that salinomycin-induced autophagy, as a survival mechanism, might be a potential strategy through ROS regulation in cancer therapy.
Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
ISSN
0006-291X
Keyword (Author)
ApoptosisAutophagyReactive oxygen speciesSalinomycinU2OS cells
Keyword
MITOCHONDRIAL ROS GENERATIONCANCER STEM-CELLMEDIATED AUTOPHAGYCYTOCHROME-CPATHWAYSINHIBITIONDEATHCYTOTOXICITYACTIVATIONMECHANISMS

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