Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs

Cell. 2011 Oct 14;147(2):344-57. doi: 10.1016/j.cell.2011.09.029.

Abstract

Here, we demonstrate that protein-coding RNA transcripts can crosstalk by competing for common microRNAs, with microRNA response elements as the foundation of this interaction. We have termed such RNA transcripts as competing endogenous RNAs (ceRNAs). We tested this hypothesis in the context of PTEN, a key tumor suppressor whose abundance determines critical outcomes in tumorigenesis. By a combined computational and experimental approach, we identified and validated endogenous protein-coding transcripts that regulate PTEN, antagonize PI3K/AKT signaling, and possess growth- and tumor-suppressive properties. Notably, we also show that these genes display concordant expression patterns with PTEN and copy number loss in cancers. Our study presents a road map for the prediction and validation of ceRNA activity and networks and thus imparts a trans-regulatory function to protein-coding mRNAs.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Animals
  • Gene Expression Regulation*
  • Humans
  • Mice
  • MicroRNAs / metabolism
  • PTEN Phosphohydrolase / genetics*
  • PTEN Phosphohydrolase / metabolism
  • Phosphatidylinositol 3-Kinases / metabolism
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism*
  • RNA, Untranslated / genetics
  • RNA, Untranslated / metabolism*
  • Regulatory Sequences, Ribonucleic Acid*

Substances

  • MicroRNAs
  • RNA, Messenger
  • RNA, Untranslated
  • Regulatory Sequences, Ribonucleic Acid
  • Phosphatidylinositol 3-Kinases
  • PTEN Phosphohydrolase
  • PTEN protein, human
  • Pten protein, mouse