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Antiproliferative protein Tob directly regulates c-myc proto-oncogene expression through cytoplasmic polyadenylation

K Ogami1, N Hosoda1, Y Funakoshi1

  • 1Department of Biological Chemistry, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya, Japan.

Oncogene
|November 27, 2012
PubMed

Insights

The antiproliferative protein Tob regulates c-myc gene expression by controlling mRNA deadenylation. Tob

Area of Science:

  • Molecular Biology
  • Gene Regulation
  • Cancer Biology

Background:

  • mRNA deadenylation is a key post-transcriptional gene expression control.
  • The proto-oncogene c-myc is crucial for cell growth and proliferation.

Purpose of the Study:

  • To investigate the role of the antiproliferative protein Tob in regulating c-myc gene expression.
  • To elucidate the mechanism by which Tob influences c-myc mRNA stability.

Main Methods:

  • Investigated the interaction between Tob, Caf1 deadenylase, and cytoplasmic polyadenylation element-binding protein (CPEB).
  • Analyzed the effect of the CPEB-Tob-Caf1 complex on c-myc mRNA deadenylation and decay.
  • Examined c-myc mRNA stability in quiescent versus serum-stimulated cells.

Main Results:

  • Tob, as part of the Caf1-Ccr4 deadenylase complex, binds to CPEB to form a ternary complex.
  • This complex (CPEB-Tob-Caf1) accelerates c-myc mRNA deadenylation and decay, suppressing its expression.
  • Upon serum stimulation, Tob and Caf1 release from CPEB, stabilizing c-myc mRNA for rapid induction.

Conclusions:

  • Tob is a critical regulator of c-myc gene expression, essential for cell growth.
  • Tob controls cell growth, at least partly, by modulating c-myc expression through mRNA deadenylation.
  • The dynamic regulation of Tob-mediated c-myc expression is vital for cell cycle control.

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