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Nucleic Acids Research Advance Access published online on October 13, 2009
Nucleic Acids Research, doi:10.1093/nar/gkp755
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© The Author(s) 2009. Published by Oxford University Press.
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.5/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

RNA

Stabilization of XIAP mRNA through the RNA binding protein HuR regulated by cellular polyamines

Xian Zhang1,2, Tongtong Zou1,2, Jaladanki N. Rao1,2, Lan Liu1,2, Lan Xiao1,3, Peng-Yuan Wang1,3, Yu-Hong Cui1,2, Myriam Gorospe4 and Jian-Ying Wang1,2,3,*

1Cell Biology Group, Department of Surgery, University of Maryland School of Medicine, 2Baltimore Veterans Affairs Medical Center, 3Department of Pathology, University of Maryland School of Medicine and 4Laboratory of Cellular and Molecular Biology, National Institute on Aging-IRP, NIH, Baltimore, MD 21224, USA

*To whom correspondence should be addressed. Tel: +1 410 605 7000 (ext. 5678); Fax: +1 410 605 7919; Email: jwang{at}smail.umaryland.edu

Received July 21, 2009. Revised August 26, 2009. Accepted August 27, 2009.

The X chromosome-linked inhibitor of apoptosis protein (XIAP) is the most potent intrinsic caspase inhibitor and plays an important role in the maintenance of intestinal epithelial integrity. The RNA binding protein, HuR, regulates the stability and translation of many target transcripts. Here, we report that HuR associated with both the 3'-untranslated region and coding sequence of the mRNA encoding XIAP, stabilized the XIAP transcript and elevated its expression in intestinal epithelial cells. Ectopic HuR overexpression or elevated cytoplasmic levels of endogenous HuR by decreasing cellular polyamines increased [HuR/XIAP mRNA] complexes, in turn promoting XIAP mRNA stability and increasing XIAP protein abundance. Conversely, HuR silencing in normal and polyamine-deficient cells rendered the XIAP mRNA unstable, thus reducing the steady state levels of XIAP. Inhibition of XIAP expression by XIAP silencing or by HuR silencing reversed the resistance of polyamine-deficient cells to apoptosis. Our findings demonstrate that HuR regulates XIAP expression by stabilizing its mRNA and implicates HuR-mediated XIAP in the control of intestinal epithelial apoptosis.

Present address: Xian Zhang, Guangzhou Provincial Hospital of Traditional Chinese Medicine, Guangzhou 510120, China.


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