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Nucleic Acids Research Advance Access originally published online on November 5, 2007
Nucleic Acids Research 2008 36(1):51-66; doi:10.1093/nar/gkm942
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Nucleic Acids Research, 2008, Vol. 36, No. 1 51-66
© 2007 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

Nuclear receptor interaction protein, a coactivator of androgen receptors (AR), is regulated by AR and Sp1 to feed forward and activate its own gene expression through AR protein stability

Pei-Hong Chen1, Yeou-Ping Tsao2, Chih-Chiang Wang1 and Show-Li Chen1,*

1Graduate Institute of Microbiology, College of Medicine, National Taiwan University, Taipei 100 and 2Department of Ophthalmology, Mackay Memorial Hospital; Taipei 104, Taiwan

*To whom correspondence should be addressed. Tel: +886 2 23123456 ext 8289; Fax: +886 2 2391 5293; Email: showlic{at}ntu.edu.tw

Received August 8, 2007. Revised October 11, 2007. Accepted October 11, 2007.

Previously, we found a novel gene, nuclear receptor interaction protein (NRIP), a transcription cofactor that can enhance an AR-driven PSA promoter activity in a ligand-dependent manner in prostate cancer cells. Here, we investigated NRIP regulation. We cloned a 413-bp fragment from the transcription initiation site of the NRIP gene that had strong promoter activity, was TATA-less and GC-rich, and, based on DNA sequences, contained one androgen response element (ARE) and three Sp1-binding sites (Sp1-1, Sp1-2, Sp1-3). Transient promoter luciferase assays, chromatin immunoprecipitation and small RNA interference analyses mapped ARE and Sp1-2-binding sites involved in NRIP promoter activation, implying that NRIP is a target gene for AR or Sp1. AR associates with the NRIP promoter through ARE and indirectly through Sp1-binding site via AR–Sp1 complex formation. Thus both ARE and Sp1-binding site within the NRIP promoter can respond to androgen induction. More intriguingly, NRIP plays a feed-forward role enhancing AR-driven NRIP promoter activity via NRIP forming a complex with AR to protect AR protein from proteasome degradation. This is the first demonstration that NRIP is a novel AR-target gene and that NRIP expression feeds forward and activates its own expression through AR protein stability.


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[Abstract] [Full Text] [PDF]


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