Depletion of mitochondrial fission factor DRP1 causes increased apoptosis in human colon cancer cells
Depletion of mitochondrial fission factor DRP1 causes increased apoptosis in human colon cancer cells
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DOI：
10.1016/j.bbrc.2012.03.118
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发表时间：
2012-04-27
影响因子：
3.1
通讯作者：
Oda, Hideaki
中科院分区：
文献类型：
--
作者：
Inoue-Yamauchi, Akane;Oda, Hideaki
Mitochondria play a critical role in regulation of apoptosis, a form of programmed cell death, by releasing apoptogenic factors including cytochrome c. Growing evidence suggests that dynamic changes in mitochondrial morphology are involved in cellular apoptotic response. However, whether DRP1-mediated mitochondrial fission is required for induction of apoptosis remains speculative. Here, we show that siRNA-mediated DRP1 knockdown promoted accumulation of elongated mitochondria in HCT116 and SW480 human colon cancer cells. Surprisingly, DRP1 down-regulation led to decreased proliferation and increased apoptosis of these cells. A higher rate of cytochrome c release and reductions in mitochondrial membrane potential were also revealed in DRP1-depleted cells. Taken together, our present findings suggest that mitochondrial fission factor DRP1 inhibits colon cancer cell apoptosis through the regulation of cytochrome c release and mitochondrial membrane integrity. (C) 2012 Elsevier Inc. All rights reserved.
