Journal
CELL DEATH AND DIFFERENTIATION
Volume 13, Issue 12, Pages 2062-2067Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/sj.cdd.4401968
Keywords
apoptosis; cytochrome c; cancer; DNA damage
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Funding
- NCI NIH HHS [CA-13106-31] Funding Source: Medline
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During apoptosis, cytochrome c released from mitochondria activates Apaf-1, a cofactor of caspase-9. The evidence that cytochrome c can activate Apaf-1 is abundant, but the proof that cytochrome c is required for apoptosis is limited to two studies that used genetically modified mice. One of these studies concluded that in some tissues apoptosis may require Apaf-1 but not cytochrome c, which indicated the need to analyze the requirement of cytochrome c beyond the mouse models, and in human tumor cells in particular. In this study, we designed tools to silence cytochrome c expression in human cells and tested these tools in an experimental system of oncogenic transformation. We found that cytochrome c was required for apoptosis induced by both DNA damage and, unexpectedly, TNF alpha. Overall, this study established that cytochrome c is required for apoptosis in human cells and provided tools to dissect mechanisms of apoptosis in various experimental models.
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