Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/26715
Title: Daxx regulates mitotic progression and prostate cancer predisposition
Authors: Kwan, PS
Lau, CC
Chiu, YT
Man, C
Liu, J
Tang, KD
Wong, YC
Ling, MT
Issue Date: 2013
Publisher: Oxford Univ Press
Source: Carcinogenesis, 2013, v. 34, no. 4, p. 750-759 How to cite?
Journal: Carcinogenesis 
Abstract: Mitotic progression of mammalian cells is tightly regulated by the E3 ubiquitin ligase anaphase promoting complex (APC)/C. Deregulation of APC/C is frequently observed in cancer cells and is suggested to contribute to chromosome instability and cancer predisposition. In this study, we identified Daxx as a novel APC/C inhibitor frequently overexpressed in prostate cancer. Daxx interacts with the APC/C coactivators Cdc20 and Cdh1 in vivo, with the binding of Cdc20 dependent on the consensus destruction boxes near the N-terminal of the Daxx protein. Ectopic expression of Daxx, but not the D-box deleted mutant (DaxxΔD-box), inhibited the degradation of APC/Cdc20 and APC/Cdh1 substrates, leading to a transient delay in mitotic progression. Daxx is frequently upregulated in prostate cancer tissues; the expression level positively correlated with the Gleason score and disease metastasis (P = 0.027 and 0.032, respectively). Furthermore, ectopic expression of Daxx in a non-malignant prostate epithelial cell line induced polyploidy under mitotic stress. Our data suggest that Daxx may function as a novel APC/C inhibitor, which promotes chromosome instability during prostate cancer development.
URI: http://hdl.handle.net/10397/26715
ISSN: 0143-3334
DOI: 10.1093/carcin/bgs391
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