Abstract
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 language | English (US) |
|---|---|
| Pages (from-to) | 3039-3042 |
| Number of pages | 4 |
| Journal | Cell Cycle |
| Volume | 6 |
| Issue number | 24 |
| DOIs | |
| State | Published - Dec 15 2007 |
Funding
We thank members of the Kiyokawa laboratory for comments on the manuscript. This research was supported partly by NIH (RO1-CA100204, CA112282, and HD38085), the Department of Defense (DAMD 17-02-1-0413), the Searle Leadership Fund, the Zell Scholar Fund, and the Robert H. Lurie Comprehensive Cancer Center.
Keywords
- Breast cancer
- CDC25
- CDK
- Checkpoint
- Chk1
- Phosphatase
- Transformation
ASJC Scopus subject areas
- Molecular Biology
- Cell Biology
- Developmental Biology
