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Nucleic Acids Research Advance Access originally published online on November 6, 2006
Nucleic Acids Research 2006 34(21):6158-6169; doi:10.1093/nar/gkl834
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Nucleic Acids Research, 2006, Vol. 34, No. 21 6158-6169
© 2006 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

NSPc1 is a cell growth regulator that acts as a transcriptional repressor of p21Waf1/Cip1 via the RARE element

Yanhua Gong, Jiping Yue, Xudong Wu, Xu Wang, Jianyan Wen, Lifang Lu1, Xiaozhong Peng*, Boqin Qiang and Jiangang Yuan*

National Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and Peking Union Medical College, National Human Genome Center Beijing 100005, China 1 Shanghai Genomics, Inc. Shanghai, 201203, China

*To whom correspondence should be addressed. Tel: +86 10 65296411; Fax: +86 10 65240529; Email: pengxiaozhong{at}pumc.edu.cn

Received August 7, 2006. Revised October 8, 2006. Accepted October 8, 2006.

The mammalian polycomb group proteins play an important role in cell cycle control and tumorigenesis. Nervous system polycomb 1 (NSPc1) is a newly identified transcription repressor, highly homologous with PcG protein Bmi-1. In this article, we showed that NSPc1 could promote tumor cell cycle progression and cell proliferation. Semi-quantitative RT–PCR showed that NSPc1 did not affect the expression levels of most Cyclin-depentent kinases (CDK) inhibitors except for p21Waf1/Cip1. Repression activity assays, chromatin immunoprecipitation (ChIP) and DNA pulldown assays all verified that NSPc1 represses the expression of p21Waf1/Cip1 by binding to the (–1357 to –1083) region of the p21Waf1/Cip1 promoter in vivo, and the repression effect is dependent on the retinoid acid response element (RARE element) within the above region of the p21Waf1/Cip1 promoter. Further analysis showed that NSPc1 could compete the RARE element site with RA receptors both in vitro and in vivo. Taken together, our results support the hypothesis that NSPc1 has a positive role in tumor cell growth by down-regulating p21Waf1/Cip1 via the RARE element, which directly connects transcriptional repression of PcGs to CDKIs and RA signaling pathways.

*Correspondence may also be addressed to Jiangang Yuan. Tel: +86 10 65296411; Fax: +86 10 65240529; Email: yuanjiangang{at}pumc.edu.cn

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


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X. Wu, Y. Gong, J. Yue, B. Qiang, J. Yuan, and X. Peng
Cooperation between EZH2, NSPc1-mediated histone H2A ubiquitination and Dnmt1 in HOX gene silencing
Nucleic Acids Res., June 1, 2008; 36(11): 3590 - 3599.
[Abstract] [Full Text] [PDF]


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