Sustained activation of ERK1/2 by NGF induces microRNA-221 and 222 in PC12 cells

FEBS J. 2009 Jun;276(12):3269-76. doi: 10.1111/j.1742-4658.2009.07041.x. Epub 2009 Apr 25.

Abstract

MicroRNAs (miRNAs) are small non-coding RNAs that regulate gene expression by inhibiting translation and/or inducing degradation of target mRNAs, and they play important roles in a wide variety of biological functions including cell differentiation, tumorigenesis, apoptosis and metabolism. However, there is a paucity of information concerning the regulatory mechanism of miRNA expression. Here we report identification of growth factor-regulated miRNAs using the PC12 cell line, an established model of neuronal growth and differentiation. We found that expression of miR-221 and miR-222 expression were induced by nerve growth factor (NGF) stimulation in PC12 cells, and that this induction was dependent on sustained activation of the extracellular signal-regulated kinase 1 and 2 (ERK1/2) pathway. Using a target prediction program, we also identified a pro-apototic factor, the BH3-only protein Bim, as a potential target of miR-221/222. Overexpression of miR-221 or miR-222 suppressed the activity of a luciferase reporter activity fused to the 3' UTR of Bim mRNA. Furthermore, overexpression of miR-221/222 decreased endogenous Bim mRNA expression. These results reveal that the ERK signal regulates miR-221/222 expression, and that these miRNAs might contribute to NGF-dependent cell survival in PC12 cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 5' Untranslated Regions / genetics
  • Animals
  • Apoptosis Regulatory Proteins / genetics
  • Base Sequence
  • Bcl-2-Like Protein 11
  • Blotting, Western
  • Butadienes / pharmacology
  • Cycloheximide / pharmacology
  • Enzyme Inhibitors / pharmacology
  • Gene Expression / drug effects
  • Luciferases / genetics
  • Luciferases / metabolism
  • Membrane Proteins / genetics
  • MicroRNAs / genetics*
  • MicroRNAs / metabolism
  • Mitogen-Activated Protein Kinase 1 / antagonists & inhibitors
  • Mitogen-Activated Protein Kinase 1 / metabolism*
  • Mitogen-Activated Protein Kinase 3 / antagonists & inhibitors
  • Mitogen-Activated Protein Kinase 3 / metabolism*
  • Nerve Growth Factor / pharmacology*
  • Nitriles / pharmacology
  • PC12 Cells
  • Protein Biosynthesis / drug effects
  • Protein Synthesis Inhibitors / pharmacology
  • Proto-Oncogene Proteins / genetics
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Rats
  • Recombinant Fusion Proteins / genetics
  • Recombinant Fusion Proteins / metabolism
  • Reverse Transcriptase Polymerase Chain Reaction
  • Sequence Homology, Nucleic Acid
  • Signal Transduction / drug effects
  • Time Factors

Substances

  • 5' Untranslated Regions
  • Apoptosis Regulatory Proteins
  • Bcl-2-Like Protein 11
  • Bcl2l11 protein, rat
  • Butadienes
  • Enzyme Inhibitors
  • Membrane Proteins
  • MicroRNAs
  • Nitriles
  • Protein Synthesis Inhibitors
  • Proto-Oncogene Proteins
  • RNA, Messenger
  • Recombinant Fusion Proteins
  • U 0126
  • Nerve Growth Factor
  • Cycloheximide
  • Luciferases
  • Mitogen-Activated Protein Kinase 1
  • Mitogen-Activated Protein Kinase 3