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Salinomycin induces reactive oxygen species and apoptosis in aggressive breast cancer cells as mediated with regulation of autophagy

Author(s)
Kim, Kwang-YounPark, Kwang IlKim, Sang-HunYu, Sun-NyoungLee, DeokjaeKim, Young WooNoh, Kyung TaeMa, Jin YeulSeo, Young KyoAhn, Soon-Cheol
Issued Date
2017-04
DOI
10.21873/anticanres.11507
URI
https://scholarworks.unist.ac.kr/handle/201301/21924
Fulltext
http://ar.iiarjournals.org/content/37/4/1747.abstract
Citation
ANTICANCER RESEARCH, v.37, no.4, pp.1747 - 1758
Abstract
Background/Aim: Chemotherapy is a critical option for cancer treatment. However, consistent exposure to chemotherapeutic drugs promotes chemoresistance in cancer cells through diverse mechanisms. Accordingly, we investigated whether salinomycin, a monocarboxylic ionophore, could induce apoptosis in aggressive breast cancer cells or not, as well as its underlying mechanism. Materials and Methods: Using salinomycin on two breast cancer cell lines, MCF-7 cells and MDA-MB-231 cells, cell viability, annexin V/propidium iodide staining, acridine orange staining, caspase-3/9 activity, reactive oxygen species (ROS) and mitochondrial membrane potential (MMP) were assayed. Results: In this study, salinomycin induced apoptosis and autophagy in MDA-MB-231 cells. Salinomycin-mediated ROS production led to mitochondrial dysfunction in MDA-MB-231 cells. Interestingly, treatment of N-acetyl-L-cysteine (NAC), a scavenger of ROS, attenuated salinomycin-induced apoptosis and autophagy. Moreover, autophagy inhibition is involved in acceleration of apoptosis induced by salinomycin. Conclusion: Salinomycin induced apoptosis and ROS production, that were blocked by autophagy, thus resulting in protecting cancer cells. This crosstalk of two different physiological responses (autophagy and apoptosis) induced by salinomycin might play pivotal roles in the relationship between autophagy and apoptosis of cancer cells.
Publisher
INT INST ANTICANCER RESEARCH
ISSN
0250-7005
Keyword (Author)
ROSautophagyapoptosisbreast cancerchemoresistancesalinomycin
Keyword
DEATHDOXORUBICINSTATISTICSACTIVATIONP21

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