LincRNA-p21 suppresses target mRNA translation

Mol Cell. 2012 Aug 24;47(4):648-55. doi: 10.1016/j.molcel.2012.06.027. Epub 2012 Jul 26.

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.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Base Sequence
  • Carboxypeptidases / genetics
  • Carboxypeptidases / metabolism
  • ELAV Proteins / genetics
  • ELAV Proteins / metabolism
  • HeLa Cells
  • Humans
  • MicroRNAs / genetics
  • Molecular Sequence Data
  • Protein Biosynthesis*
  • Proteolysis
  • RNA Processing, Post-Transcriptional*
  • RNA, Long Noncoding / genetics*
  • RNA, Messenger / genetics
  • RNA-Binding Proteins / genetics
  • RNA-Binding Proteins / metabolism
  • Transcription, Genetic
  • Tumor Cells, Cultured
  • beta Catenin / genetics
  • beta Catenin / metabolism

Substances

  • CTNNB1 protein, human
  • ELAV Proteins
  • MicroRNAs
  • RNA, Long Noncoding
  • RNA, Messenger
  • RNA-Binding Proteins
  • beta Catenin
  • mirnlet7 microRNA, human
  • Carboxypeptidases
  • SCPEP1 protein, human