Department of Molecular Science & Technology, Institute for Medical Sciences, Ajou University School of Medicine, Suwon 443-749, Republic of Korea.
Cancer Lett. 2012 Nov 28;324(2):197-209. doi: 10.1016/j.canlet.2012.05.018. Epub 2012 May 22.
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.
在这项研究中，我们研究了 Ca(2+) 在姜黄素诱导的细胞程序性坏死中的作用，程序性坏死是一种伴随着线粒体和内质网（ER）扩张的细胞死亡方式。姜黄素选择性地诱导恶性乳腺癌细胞中线粒体 Ca(2+)超载，而不是正常乳腺细胞，导致线粒体/ER 扩张和随后的细胞程序性坏死。此外，我们发现同时抑制线粒体 Na(+)/Ca(2+)交换器（mNCX）和蛋白酶体可以引发持续的线粒体 Ca(2+)超载，并有效地诱导恶性乳腺癌细胞发生细胞程序性坏死。
