期刊
CELL DEATH AND DIFFERENTIATION
卷 19, 期 4, 页码 573-581出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/cdd.2011.126
关键词
Pdcd4; caspase-3; microRNA; translational control
资金
- Ministry of Education, Science, Sports, and Culture of Japan [22247008]
- Grants-in-Aid for Scientific Research [22247008] Funding Source: KAKEN
The programmed cell death 4 (Pdcd4), a translation inhibitor, plays an essential role in tumor suppression, but its role in apoptosis remains unclear. Here we show that Pdcd4 is a critical suppressor of apoptosis by inhibiting the translation of procaspase-3 mRNA. Pdcd4 protein decreased more rapidly through microRNA-mediated translational repression following apoptotic stimuli than did the activation of procaspase-3, cleavage of poly(ADP) ribose polymerase (PARP) by active caspase-3, and nuclear fragmentation. Strikingly, the loss of Pdcd4 by the specific RNA interference increased procaspase-3 expression, leading to its activation and PARP cleavage even without apoptotic stimuli, and sensitized the cells to apoptosis. Thus, our findings provide insight into a novel mechanism for Pdcd4 as a regulator of apoptosis. Cell Death and Differentiation (2012) 19, 573-581; doi:10.1038/cdd.2011.126; published online 30 September 2011
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