Depletion of mitochondrial fission factor DRP1 causes increased apoptosis in human colon cancer cells

作者：Inoue Yamauchi Akane^*; Oda Hideaki

来源：Biochemical and Biophysical Research Communications, 2012, 421(1): 81-85.

DOI：10.1016/j.bbrc.2012.03.118

• DRP1
• Apoptosis
• Colon cancer cell

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.

• 出版日期2012-4-27