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Down-regulation of IDH2 sensitizes cancer cells to erastin-induced ferroptosis

Authors
Kim, HyunjinLee, Jin HyupPark, Jeen-Woo
Issue Date
30-4월-2020
Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
Keywords
Ferroptosis; IDH2; Erastin; Sensitization
Citation
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.525, no.2, pp.366 - 371
Indexed
SCIE
SCOPUS
Journal Title
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume
525
Number
2
Start Page
366
End Page
371
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/56259
DOI
10.1016/j.bbrc.2020.02.093
ISSN
0006-291X
Abstract
Ferroptosis is a form of regulated cell death induced by lipid peroxidation that is dependent on iron. This pathway is being considered as an alternative anticancer therapeutic strategy, and the chemoreagent erastin induces ferroptosis by blocking system Xc(-), which causes a cysteine shortage that depletes intracellular GSH. Mitochondrial NADP(+)-dependent isocitrate dehydrogenase (IDH2) is major enzyme that produces NADPH, which is a crucial source for mitochondrial GSH turnover. Therefore, we hypothesized that down-regulation of IDH2 would have a synergic effect on erastin-induced ferroptosis. Here, we investigated the effect of IDH2 knockdown on ferroptosis in human HT1080 fibrosarcoma and murine Hepa1-6 hepatoma cells cultured in vitro as well as in an in vivo model of allografted Hepa1-6 cells in nude mice. Our results show that susceptibility to ferroptosis was substantially increased when IDH2 was down-regulated. This study supports that IDH2 has protective effect against ferroptotic cell death, and that the enzyme could be targeted to sensitize cancer cells to ferroptosis. (C) 2020 Elsevier Inc. All rights reserved.
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