| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 1996504 | Molecular Cell | 2012 | 8 Pages |
SummaryMammalian long intergenic noncoding RNAs (lincRNAs) are best known for modulating transcription. Here we report a posttranscriptional function for lincRNA-p21 as a modulator of translation. Association of the RNA-binding protein HuR with lincRNA-p21 favored the recruitment of let-7/Ago2 to lincRNA-p21, leading to lower lincRNA-p21 stability. Under reduced HuR levels, lincRNA-p21 accumulated in human cervical carcinoma HeLa cells, increasing its association with JUNB and CTNNB1 mRNAs and selectively lowering their translation. With elevated HuR, lincRNA-p21 levels declined, which in turn derepressed JunB and β-catenin translation and increased the levels of these proteins. We propose that HuR controls translation of a subset of target mRNAs by influencing lincRNA-p21 levels. Our findings uncover a role for lincRNA as a posttranscriptional inhibitor of translation.
► RNA-binding protein HuR recruits let-7 to lincRNA-p21, lowers lincRNA-p21 stability ► lincRNA-p21 selectively binds JUNB and CTNNB1 mRNAs, represses their translation ► With low HuR, lincRNA-p21 levels rise, repressing JunB and β-catenin translation ► With high HuR, lincRNA-p21 levels decline, rising JunB and β-catenin translation
