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Simultaneous mitochondrial Ca2+ overload and proteasomal inhibition are responsible for the induction of paraptosis in malignant breast cancer cells

Authors
Yoon, Mi JinKim, Eun HeeKwon, Taeg KyuPark, Sun AhChoi, Kyeong Sook
Issue Date
28-Nov-2012
Publisher
Elsevier BV
Keywords
Paraptosis; Curcumin; Mitochondrial Ca2+; Proteasomal inhibition; Breast cancer
Citation
Cancer Letters, v.324, no.2, pp 197 - 209
Pages
13
Journal Title
Cancer Letters
Volume
324
Number
2
Start Page
197
End Page
209
URI
https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/14691
DOI
10.1016/j.canlet.2012.05.018
ISSN
0304-3835
1872-7980
Abstract
In this study, we investigated the role of Ca2+ in curcumin-induced paraptosis, a cell death mode that is accompanied by dilation of mitochondria and the endoplasmic reticulum (ER). Curcumin induced mitochondria! Ca2+ overload selectively in the malignant breast cancer cells, but not in the normal breast cell, contributing to the dilation of mitochondria/ER and subsequent paraptotic cell death. In addition, we found that simultaneous inhibition of the mitochondrial Na+/Ca2+ exchanger (mNCX) and proteasomes can trigger a sustained mitochondrial Ca2+ overload and effectively induce paraptosis in malignant breast cancer cells. (C) 2012 Elsevier Ireland Ltd. All rights reserved.
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