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Mol Cell Biol. 2011 Jan;31(1):215-25. doi: 10.1128/MCB.01031-10. Epub 2010 Oct 25.

Posttranscriptional suppression of proto-oncogene c-fms expression by vigilin in breast cancer.

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  • 1Arizona Cancer Center, University of Arizona, Tucson, AZ 85724, USA. hwoo@azcc.arizona.edu

Abstract

cis-acting elements found in 3'-untranslated regions (UTRs) are regulatory signals determining mRNA stability and translational efficiency. By binding a novel non-AU-rich 69-nucleotide (nt) c-fms 3' UTR sequence, we previously identified HuR as a promoter of c-fms proto-oncogene mRNA. We now identify the 69-nt c-fms mRNA 3' UTR sequence as a cellular vigilin target through which vigilin inhibits the expression of c-fms mRNA and protein. Altering association of either vigilin or HuR with c-fms mRNA in vivo reciprocally affected mRNA association with the other protein. Mechanistic studies show that vigilin decreased c-fms mRNA stability. Furthermore, vigilin inhibited c-fms translation. Vigilin suppresses while HuR encourages cellular motility and invasion of breast cancer cells. In summary, we identified a competition for binding the 69-nt sequence, through which vigilin and HuR exert opposing effects on c-fms expression, suggesting a role for vigilin in suppression of breast cancer progression.

PMID:
20974809
[PubMed - indexed for MEDLINE]
PMCID:
PMC3019847
Free PMC Article
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