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In vivo significance of the G2 restriction point

Floris Foijer1, Elly Delzenne-Goette, Marleen Dekker

  • 1Division of Molecular Biology, The Netherlands Cancer Institute, Amsterdam, the Netherlands.

Cancer Research
|October 3, 2007
PubMed

Insights

Retinoblastoma (Rb) loss in the pituitary activates a G2 restriction point, indicated by cyclin B1-p27KIP1 complexes. These complexes persist in Rb-deficient tumors, suggesting the G2 checkpoint retards, but does not prevent, pituitary tumor growth.

Area of Science:

  • Oncology
  • Cell Biology
  • Molecular Biology

Background:

  • Loss of the retinoblastoma (Rb) pathway is common in human cancers.
  • Mouse models show Rb loss accelerates tumorigenesis when p27KIP1 is also lost, potentially due to G1 checkpoint weakening.
  • The role of p27KIP1 in the G2 restriction point offers an alternative explanation for this synergy.

Purpose of the Study:

  • To investigate the significance of the G2 restriction point in Rb-deficient pituitary glands.
  • To determine if the G2 restriction point operates in vivo in the context of Rb loss.
  • To understand the role of p27KIP1 in the G2 restriction point during tumorigenesis.

Main Methods:

  • Analysis of Rb-deficient pituitary glands.
  • Detection of cyclin B1-p27KIP1 complexes as a marker for G2 restriction point activation.
  • Examination of Rb-deficient tumors to assess the persistence of these complexes.

Main Results:

  • Rb loss in the pituitary gland activates the G2 restriction point.
  • Activation is evidenced by the formation of cyclin B1-p27KIP1 complexes.
  • These cyclin B1-p27KIP1 complexes were found to be present in Rb-deficient tumors.

Conclusions:

  • The G2 restriction point is operational in vivo.
  • In the pituitary gland, Rb loss leads to the activation of the G2 restriction point.
  • This G2 restriction point mechanism appears to retard, rather than prevent, tumor growth in Rb-deficient pituitaries.

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