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LincRNA-p21 Suppresses Target mRNA Translation

Molecular CellPublished 26 July 2012Open access
Je‐Hyun Yoon, Kotb Abdelmohsen, Subramanya Srikantan, Xiaoling Yang, Jennifer L. Martindale, Supriyo De
Citations975
SJR quartileQ1
SJR score9.05
SNIP2.89
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TL;DR

It is proposed that HuR controls translation of a subset of target mRNAs by influencing lincRNA-p21 levels, which in turn derepressed JunB and β-catenin translation and increased the levels of these proteins.

Abstract

Mammalian 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.

Keywords

Biochemistry, Genetics and Molecular Biology