Depletion of mitochondrial fission factor DRP1 causes increased apoptosis in human colon cancer cells.
In: Biochemical and biophysical research communications, Jg. 421 (2012-04-27), Heft 1, S. 81-5
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Zugriff:
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.
(Copyright © 2012 Elsevier Inc. All rights reserved.)
Titel: |
Depletion of mitochondrial fission factor DRP1 causes increased apoptosis in human colon cancer cells.
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Autor/in / Beteiligte Person: | Inoue-Yamauchi, A ; Oda, H |
Zeitschrift: | Biochemical and biophysical research communications, Jg. 421 (2012-04-27), Heft 1, S. 81-5 |
Veröffentlichung: | <2002- >: San Diego, CA : Elsevier ; <i>Original Publication</i>: New York, Academic Press., 2012 |
Medientyp: | academicJournal |
ISSN: | 1090-2104 (electronic) |
DOI: | 10.1016/j.bbrc.2012.03.118 |
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