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[Cancer Research 65, 6685-6691, August 1, 2005]
© 2005 American Association for Cancer Research

Cell and Tumor Biology

Ckap2 Regulates Aneuploidy, Cell Cycling, and Cell Death in a p53-Dependent Manner

Katsuya Tsuchihara1, Valentina Lapin1, Christopher Bakal2,3, Hitoshi Okada1, Lauren Brown2,3, Masami Hirota-Tsuchihara2, Kathrin Zaugg1,3, Alexandra Ho1, Annick Itie-YouTen1, Marees Harris-Brandts2, Robert Rottapel2,3, Christopher D. Richardson2,3, Samuel Benchimol2,3 and Tak Wah Mak1,2,3,4

1 The Campbell Family Institute for Breast Cancer Research, 2 Ontario Cancer Institute, and Departments of 3 Medical Biophysics and 4 Immunology, University of Toronto, Toronto, Ontario, Canada

Requests for reprints: Tak W. Mak, The Campbell Family Institute for Breast Cancer Research, 620 University Avenue, Suite 706, Toronto, Ontario, Canada M5G 2C1. Phone: 416-946-2234; Fax: 416-204-5300; E-mail: tmak{at}uhnres.utoronto.ca.

We used DNA microarray screening to identify Ckap2 (cytoskeleton associated protein 2) as a novel p53 target gene in a mouse erythroleukemia cell line. DNA damage induces human and mouse CKAP2 expression in a p53-dependent manner and p53 activates the Ckap2 promoter. Overexpressed Ckap2 colocalizes with and stabilizes microtubules. In p53-null cells, overexpression of Ckap2 induces tetraploidy with aberrant centrosome numbers, suggesting disturbed mitosis and cytokinesis. In p53-competent cells, Ckap2 does not induce tetraploidy but activates p53-mediated cell cycle arrest and apoptosis. Our data suggest the existence of a functional positive feedback loop in which Ckap2 activates the G1 tetraploidy checkpoint and prevents aneuploidy.




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