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Mol. Cell. Biol. doi:10.1128/MCB.00113-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

The RNA-binding protein HuR promotes cell migration and cell invasion by stabilizing the -actin mRNA in a U-rich-element-dependent manner

Department of Biochemistry, McGill University, Quebec, Canada; McGill Cancer Center, McGill University, Quebec, Canada

^* To whom correspondence should be addressed. Email: imed.gallouzi{at}mcgill.ca.

	Abstract

A high expression level of the beta()-actin protein is required for important biological mechanisms such as maintaining cell shape, growth and motility. Although the elevated cellular level of the -actin protein is directly linked to the long half-life of its mRNA, the molecular mechanisms responsible for this effect are unknown. Here we show that the RNA-binding protein HuR stabilizes the -actin mRNA by associating with a uridine-rich (U-rich) element within its 3'untranslated region (3'UTR). Using RNA interference to knockdown the expression of HuR in HeLa cells, we demonstrate that HuR plays an important role in the stabilization but not in the nuclear/cytoplasmic distribution of the -actin mRNA. HuR depletion in HeLa cells alters key -actin-based cytoskeleton functions such as cell adhesion, migration, and invasion, and these defects correlate with a loss of the actin stress fiber network. Together our data establish that the posttranscriptional event involving HuR-mediated--actin mRNA stabilization could be a part of the regulatory mechanisms responsible for maintaining cell integrity, which is a prerequisite to avoid transformation and tumor formation.

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