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김은희

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

Author(s)
Yoon, Mi JinKim, Eun HeeKwon, Taeg KyuPark, Sun AhChoi, Kyeong Sook
Issued Date
2012-11
DOI
10.1016/j.canlet.2012.05.018
URI
https://scholarworks.unist.ac.kr/handle/201301/20172
Fulltext
http://www.sciencedirect.com/science/article/pii/S0304383512003126
Citation
CANCER LETTERS, v.324, no.2, pp.197 - 209
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
Publisher
ELSEVIER IRELAND LTD
ISSN
0304-3835
Keyword (Author)
ParaptosisCurcuminMitochondrial Ca2+Proteasomal inhibitionBreast cancer
Keyword
ENDOPLASMIC-RETICULUM STRESSCURCUMIN INDUCES APOPTOSISOXIDATIVE STRESSIN-VITROMITOTIC CATASTROPHECALCIUMDEATHRELEASEANTICANCERACTIVATION

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