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Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols
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Direct induction of cyclin D2 by Myc contributes to cell cycle progression and sequestration of p27

C Bouchard1, K Thieke, A Maier

  • 1Institute of Molecular Biology and Tumour Research, Phillips-Universität Marburg, Emil-Mannkopff-Strasse 2, 35033 Marburg.

The EMBO Journal
|October 3, 1999
PubMed

Insights

Myc activates cyclin D2 expression, a key step in cell cycle progression. This finding reveals a novel pathway linking Myc to cell division and antagonizing cell cycle inhibitors like p27.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Oncology

Background:

  • The oncogene Myc drives cell proliferation but its downstream targets remain incompletely understood.
  • Myc's role in regulating cell cycle progression is complex, involving interactions with cyclin-dependent kinases (CDKs) and inhibitors like p27(kip1).

Purpose of the Study:

  • To identify the direct target genes of Myc responsible for inducing cell cycle progression.
  • To elucidate the mechanism by which Myc antagonizes cell cycle inhibitors and promotes cell division.

Main Methods:

  • Analysis of cyclin D2 promoter activity in response to Myc activation.
  • Chromatin immunoprecipitation to assess Myc binding to the cyclin D2 promoter.
  • Functional inhibition of cyclin D2 using p16 or antibodies.
  • Assessment of Myc-induced cell cycle entry, senescence, and apoptosis in cyclin D2-deficient fibroblasts.

Main Results:

  • Myc directly induces cyclin D2 expression by de-repressing its promoter, which is normally repressed by Mad-Max complexes.
  • Cyclin D2 is sequestered by cyclin D2-Cdk4 complexes upon Myc activation, facilitating the dissociation of p27(kip1) from Cdk2.
  • Inhibition of cyclin D2 blocks Myc-induced cell cycle entry and Myc-deficient fibroblasts exhibit accelerated senescence.

Conclusions:

  • Cyclin D2 is a direct downstream effector of Myc, mediating its ability to drive cell cycle progression.
  • This pathway involving Myc, cyclin D2, and p27(kip1) is crucial for overcoming cell cycle arrest and promoting cellular immortalization.

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