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Nucleic Acids Research Advance Access originally published online on August 9, 2008
Nucleic Acids Research 2008 36(16):5335-5349; doi:10.1093/nar/gkn504
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Nucleic Acids Research, 2008, Vol. 36, No. 16 5335-5349
© 2008 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Molecular Biology

N-Myc downstream-regulated gene 2 is involved in p53-mediated apoptosis

Na Liu1, Lifeng Wang1, Xia Li1, Qi Yang1, Xinping Liu1, Jing Zhang1, Jian Zhang1, Yousheng Wu1, Shaoping Ji1, Yingqi Zhang2, Angang Yang3, Hua Han4 and Libo Yao1,*

1Department of Biochemistry and Molecular Biology, State Key Laboratory of Cancer Biology, 2Biotechnology Center, 3Department of Immunology and 4Department of Medical Genetics and Developmental Biology, The Fourth Military Medical University, Xi’an, 710032, China

*To whom correspondence should be addressed. Tel/Fax: +86 29 84774513; Email: bioyao{at}fmmu.edu.cn

Received March 21, 2008. Revised June 25, 2008. Accepted July 22, 2008.

The tumor suppressor, p53, is a transcription factor which can modulate the transcription of a number of target genes that are involved in cell-cycle arrest and apoptosis. However, the apoptotic pathway mediated by p53 is not fully understood. Here, we showed that N-Myc downstream-regulated gene 2 (NDRG2) is a new target gene that is regulated by p53. NDRG2 mRNA and protein levels can be upregulated in a p53-dependent manner. The first intron of the NDRG2 gene contains a site that binds p53 directly and mediates wild-type p53-dependent transactivation. In addition, silencing of NDRG2 attenuates p53-mediated apoptosis, whereas overexpression of NDRG2 suppresses tumor cell growth, regardless of the presence or absence of p53. Our results indicate that NDRG2 is a novel p53-inducible target that is involved in the p53-mediated apoptosis pathway.

The authors wish it to be known that, in their opinion, the first three authors should be regarded as joint First Authors.


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