CDC25A levels determine the balance of proliferation and checkpoint response

Dipankar Ray, Hiroaki Kiyokawa*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

33 Scopus citations


Current evidence suggests that CDC25A is not only a major regulator of both G1/S and G2/M transition during unperturbed cell cycle progression, but also a critical checkpoint mediator. While CDC25A is overexpressed in a variety of human cancers, a key question remained unanswered whether such overexpression of this CDK-activating phosphatase was a mechanism or consequence of accelerated proliferation and other malignant phenotypes. Recent studies on the tumor suppressive roles of checkpoint proteins suggest that overriding checkpoint response leads normal or pre-cancerous cells to genomic instability and cumulative malignant changes. Here we provide our views on the role of CDC25A in cancer development and genomic stability, discussing insights from our recent studies on Cdc25A knockout mice and MMTV-CDC25A transgenic mice.

Original languageEnglish (US)
Pages (from-to)3039-3042
Number of pages4
JournalCell Cycle
Issue number24
StatePublished - Dec 15 2007


  • Breast cancer
  • CDC25
  • CDK
  • Checkpoint
  • Chk1
  • Phosphatase
  • Transformation

ASJC Scopus subject areas

  • Molecular Biology
  • Developmental Biology
  • Cell Biology


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