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Cyclins D1 and D2 mediate myc-induced proliferation via sequestration of p27(Kip1) and p21(Cip1)

I Perez-Roger1, S H Kim, B Griffiths

  • 1Imperial Cancer Research Fund, 44 Lincoln's Inn Fields, London WC2A 3PX, UK.

The EMBO Journal
|October 3, 1999
PubMed

Insights

Myc induces cell proliferation by increasing cyclin D1/D2 synthesis, which sequesters cell cycle inhibitors. Cyclin D1/D2 are essential for Myc-driven proliferation but not for apoptosis.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Oncology

Background:

  • Cyclin E-Cdk2 kinase activation is crucial for Myc-induced proliferation.
  • This process is thought to involve sequestration of G(1) cell cycle inhibitors (CKIs) like p27(Kip1) and p21(Cip1).

Purpose of the Study:

  • To investigate the role of cyclin D1 and cyclin D2 in Myc-induced cell proliferation.
  • To determine if cyclin D proteins mediate the sequestration of CKIs in response to Myc.

Main Methods:

  • Biochemical assays to assess protein synthesis and kinase activity.
  • Genetic analysis using knockout mouse embryonic cells (cyclin D1-/- and cyclin D2-/-).
  • Rescue experiments using retroviral expression of cyclin D1, D2, or a mutant form.

Main Results:

  • Myc induces increased synthesis rates of cyclin D1 and/or cyclin D2.
  • Primary cells lacking cyclin D1/D2 do not proliferate in response to Myc, unlike wild-type cells.
  • Restoration of cyclin D1/D2 expression rescues Myc-induced proliferation in knockout cells.

Conclusions:

  • Cyclin D1 and cyclin D2 protein synthesis is essential for Myc-induced cell proliferation.
  • The sequestration of cell cycle inhibitors by D cyclins is critical for Myc-driven cell cycle progression.
  • The sequestration function of D cyclins is dispensable for Myc-induced apoptosis.

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