Simultaneous mitochondrial Ca(2+) overload and proteasomal inhibition are responsible for the induction of paraptosis in malignant breast cancer cells.

Abstract	In this study, we investigated the role of Ca(2+) in curcumin-induced paraptosis, a cell death mode that is accompanied by dilation of mitochondria and the endoplasmic reticulum (ER). Curcumin induced mitochondrial Ca(2+) 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(+)/Ca(2+) exchanger (mNCX) and proteasomes can trigger a sustained mitochondrial Ca(2+) overload and effectively induce paraptosis in malignant breast cancer cells.
Authors	Mi Jin Yoon, Eun Hee Kim, Taeg Kyu Kwon, Sun Ah Park, Kyeong Sook Choi
Journal	Cancer letters (Cancer Lett) Vol. 324 Issue 2 Pg. 197-209 (Nov 28 2012) ISSN: 1872-7980 [Electronic] Ireland
PMID	22634500 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Copyright	Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.
Chemical References	Antineoplastic Agents, Phytogenic Boronic Acids Protease Inhibitors Proteasome Inhibitors Pyrazines Sodium-Calcium Exchanger Thiazepines Clonazepam Bortezomib CGP 37157 Proteasome Endopeptidase Complex Curcumin Calcium
Topics	Antineoplastic Agents, Phytogenic (pharmacology) Antineoplastic Combined Chemotherapy Protocols (pharmacology) Boronic Acids (pharmacology) Bortezomib Breast Neoplasms (enzymology, pathology) Calcium (metabolism) Cell Death (drug effects) Cell Line, Tumor Clonazepam (analogs & derivatives, pharmacology) Curcumin (pharmacology) Dose-Response Relationship, Drug Endoplasmic Reticulum (drug effects, metabolism, pathology) Female Humans Mitochondria (drug effects, metabolism, pathology) Protease Inhibitors (pharmacology) Proteasome Endopeptidase Complex (metabolism) Proteasome Inhibitors Pyrazines (pharmacology) Sodium-Calcium Exchanger (antagonists & inhibitors, metabolism) Thiazepines (pharmacology) Time Factors

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