LincRNA-p21 Suppresses Target mRNA Translation
Copyright policy )LincRNA-p21 Suppresses Target mRNA Translation
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.
- Dignity Health United States
- MRC Laboratory of Molecular Biology United Kingdom
- National Institute of Health Pakistan
- FUNDACION PARA LA INVESTIGACION MEDICA APLICADA FIMA Spain
- National Institutes of Health United States
Base Sequence, Transcription, Genetic, Molecular Sequence Data, RNA-Binding Proteins, Cell Biology, Carboxypeptidases, MicroRNAs, ELAV Proteins, Protein Biosynthesis, Proteolysis, Tumor Cells, Cultured, Humans, RNA, Long Noncoding, RNA, Messenger, RNA Processing, Post-Transcriptional, Molecular Biology, beta Catenin, HeLa Cells
Base Sequence, Transcription, Genetic, Molecular Sequence Data, RNA-Binding Proteins, Cell Biology, Carboxypeptidases, MicroRNAs, ELAV Proteins, Protein Biosynthesis, Proteolysis, Tumor Cells, Cultured, Humans, RNA, Long Noncoding, RNA, Messenger, RNA Processing, Post-Transcriptional, Molecular Biology, beta Catenin, HeLa Cells
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