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Nucleic Acids Research 2006 34(7):2046-2055; doi:10.1093/nar/gkl150
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Published online 14 April 2006

© The Author 2006. Published by Oxford University Press. All rights reserved
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions@oxfordjournals.org

Article

Novel link between E2F1 and Smac/DIABLO: proapoptotic Smac/DIABLO is transcriptionally upregulated by E2F1

Wei Xie, Peng Jiang, Lin Miao, Ying Zhao1, Zhai Zhimin2, Li Qing2, Wei-guo Zhu1 and Mian Wu*

Hefei National Laboratory for Physical Sciences at Microscale and School of Life Sciences, University of Science and Technology of China Hefei, Anhui, 230027, China 1 Department of Biochemistry and Molecular Biology and the Cancer Research Center, Peking University Health Science Center 38 Xueyuan Road, Beijing, 100083, China 2 Central Laboratory, Anhui Provincial Hospital Hefei, Anhui, 230001, China

*To whom correspondence should be addressed. Tel: +86 551 3607324; Fax: +86 551 3606264; Email: wumian{at}ustc.edu.cn

Received January 10, 2006. Revised January 30, 2006. Accepted March 17, 2006.

Deregulated expression of E2F1 not only promotes S-phase entry but also induces apoptosis. Although it has been well documented that E2F1 is able to induce p53-dependent apoptosis via raising ARF activity, the mechanism by which E2F induces p53-independent apoptosis remains unclear. Here we report that E2F1 can directly bind to and activate the promoter of Smac/DIABLO, a mitochondrial proapoptotic gene, through the E2F1-binding sites BS2 (–542 ~ –535 bp) and BS3 (–200 ~ –193 bp). BS2 and BS3 appear to be utilized in combination rather than singly by E2F1 in activation of Smac/DIABLO. Activation of BS2 and BS3 are E2F1-specific, since neither E2F2 nor E2F3 is able to activate BS2 or BS3. Using the H1299 ER-E2F1 cell line where E2F1 activity can be conditionally induced, E2F1 has been shown to upregulate the Smac/DIABLO expression at both mRNA and protein levels upon 4-hydroxytamoxifen treatment, resulting in an enhanced mitochondria-mediated apoptosis. Reversely, reducing the Smac/DIABLO expression by RNA interference significantly diminishes apoptosis induced by E2F1. These results may suggest a novel mechanism by which E2F1 promotes p53-independent apoptosis through directly regulating its downstream mitochondrial apoptosis-inducing factors, such as Smac/DIABLO.


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