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Ras and Myc can drive oncogenic cell proliferation through individual D-cyclins

Qunyan Yu1, Maria A Ciemerych, Piotr Sicinski

  • 1Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA.

Oncogene
|August 17, 2005
PubMed

Insights

Oncogenic pathways like Ras and Myc can signal through all three D-cyclins (cyclin D1, D2, and D3). Each cyclin D type alone is sufficient to drive oncogenic proliferation in mouse fibroblasts.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Oncology

Background:

  • D-type cyclins are key regulators of the cell cycle.
  • Oncogenic pathways often converge on D-type cyclins.
  • Specific D-cyclins are hypothesized to respond to distinct oncogenic signals (e.g., Ras via cyclin D1, Myc via cyclin D2).

Purpose of the Study:

  • To investigate the individual roles of cyclin D1, D2, and D3 in mediating oncogenic signaling.
  • To determine if each D-cyclin can independently receive signals from Ras and Myc pathways.
  • To elucidate the contribution of each D-cyclin to oncogene-induced proliferation.

Main Methods:

  • Engineered mouse fibroblasts to express only cyclin D1, only D2, or only D3 ('single-cyclin' cells).
  • Assessed the ability of these single-cyclin cells to respond to Ras and Myc oncogenic pathways.
  • Correlated findings with previous studies on cells lacking all D-cyclins.

Main Results:

  • Each D-type cyclin (D1, D2, and D3) was individually sufficient to drive oncogenic proliferation in mouse fibroblasts.
  • Ras and Myc oncogenes can impact the cell cycle machinery via all three D-cyclins.
  • Cells lacking all D-cyclins exhibit significantly reduced susceptibility to Ras and Myc oncogenesis.

Conclusions:

  • The Ras and Myc oncogenes utilize all three D-type cyclins to influence the core cell cycle machinery.
  • There is functional redundancy among D-type cyclins in mediating oncogenic proliferation.
  • D-type cyclins are critical downstream effectors of Ras and Myc in driving cancer development.

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