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CDC25 phosphatases as potential human oncogenes

K Galaktionov1, A K Lee, J Eckstein

  • 1Howard Hughes Medical Institute, Cold Spring Harbor Laboratory, NY 11724, USA.

Science (New York, N.Y.)
|September 15, 1995
PubMed

Insights

CDC25 phosphatases activate cyclin-dependent kinases (CDKs). CDC25B overexpression in human breast cancers suggests CDC25 phosphatases contribute to human cancer development.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Oncology

Background:

  • Cyclin-dependent kinases (CDKs) regulate the cell cycle.
  • CDC25 phosphatases activate CDKs by removing inhibitory phosphates.
  • The human CDC25 gene family includes CDC25A, CDC25B, and CDC25C.

Purpose of the Study:

  • To investigate the role of CDC25 phosphatases in oncogenic transformation.
  • To determine if CDC25 phosphatases contribute to human cancer development.

Main Methods:

  • Assessing oncogenic focus formation in rodent cells using human CDC25A, CDC25B, or CDC25C.
  • Introducing oncogenic Ha-RASG12V or RB1 loss.
  • Analyzing tumor characteristics in mice.
  • Quantifying CDC25B expression in human breast cancer samples.

Main Results:

  • Human CDC25A and CDC25B, but not CDC25C, cooperated with Ha-RASG12V or RB1 loss to form oncogenic foci in rodent cells.
  • Transformed cells exhibited aneuploidy, soft agar growth, and formed high-grade tumors in nude mice.
  • CDC25B was overexpressed in 32% of human primary breast cancers.

Conclusions:

  • CDC25A and CDC25B phosphatases can promote oncogenic transformation.
  • CDC25B overexpression in breast cancer suggests a role in human tumorigenesis.
  • CDC25 phosphatases are potential contributors to human cancer development.

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