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Feedback regulation of c-Myc by ribosomal protein L11

Mu-Shui Dai1, Rosalie Sears, Hua Lu

  • 1Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, Indiana 46202, USA.

Cell Cycle (Georgetown, Tex.)
|November 23, 2007
PubMed

Insights

Ribosomal protein L11 inhibits cell cycle progression by regulating the c-Myc pathway. L11 overexpression reduces c-Myc activity, while L11 reduction increases it, forming a negative feedback loop.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • Ribosomal protein L11 activates p53 by inhibiting MDM2, impacting cell cycle progression.
  • Oncoprotein c-Myc drives transcription and cell proliferation.
  • L11's role in regulating c-Myc was previously unexplored.

Purpose of the Study:

  • To investigate the inhibitory effect of ribosomal protein L11 on the c-Myc pathway.
  • To elucidate the mechanism by which L11 regulates c-Myc activity and levels.
  • To understand the implications of L11-mediated c-Myc regulation in cell cycle control.

Main Methods:

  • Overexpression and knockdown of ribosomal protein L11.
  • Analysis of c-Myc-induced transcription and cell proliferation.
  • Investigation of L11 binding to c-Myc and its effect on coactivator TRRAP.
  • Assessment of histone H4 acetylation at c-Myc target gene promoters.
  • Measurement of c-Myc mRNA and protein levels following L11 manipulation.

Main Results:

  • Overexpression of L11 inhibits c-Myc-induced transcription and proliferation.
  • Reduction of endogenous L11 enhances c-Myc activities.
  • L11 competes with TRRAP for c-Myc binding via Myc box II, reducing histone acetylation.
  • L11 knockdown leads to increased mRNA and protein levels of c-Myc.
  • A negative feedback loop exists where c-Myc targets L11 transcriptionally.

Conclusions:

  • Ribosomal protein L11 inhibits cell cycle progression by regulating the c-Myc pathway.
  • L11 acts as a negative regulator of c-Myc, impacting its transcriptional activity, target gene acetylation, and protein levels.
  • The findings reveal a novel mechanism of cell cycle control involving L11 and c-Myc, with implications for cancer research.

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