Loss of ΔNp63α promotes mitotic exit in epithelial cells

被引:11
|
作者
Hau, Pok Man [1 ]
Yip, Yim Ling [1 ]
Huen, Michael S. Y. [2 ,3 ]
Tsao, Sai Wah [1 ]
机构
[1] Univ Hong Kong, Dept Anat, Li Ka Shing Fac Med, Hong Kong, Hong Kong, Peoples R China
[2] Univ Hong Kong, Genome Stabil Res Lab, Dept Anat, Hong Kong, Hong Kong, Peoples R China
[3] Univ Hong Kong, Ctr Canc Res, Hong Kong, Hong Kong, Peoples R China
关键词
Cell cycle; p63; Mitosis; STEM-CELLS; AURORA-A; P63; CANCER; GENE; IDENTIFICATION; PROLIFERATION; TARGETS; MITOSIS; CYCLE;
D O I
10.1016/j.febslet.2011.07.030
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Protein p63 is a key regulator in cell proliferation and cell differentiation in stratified squamous epithelium. Delta Np63 alpha is the most commonly expressed p63 isoform, which is often overexpressed in human tumor. In the present work we report the potential involvement of Delta Np63 alpha in cell cycle regulation. Delta Np63 alpha accumulated in mitotic cells but its expression decreased during mitotic exit. Moreover, Delta Np63 alpha knockdown promoted mitotic exit. Delta Np63 alpha shares a conserved destruction box (D-box) motif with other potential targets of the Anaphase-Promoting Complex/Cyclosome (APC/C). Overexpression of APC/C coactivator Cdh1 destabilized Delta Np63 alpha. Our results suggest that Delta Np63 alpha level is cell cycle-regulated and may play a role in the regulation of mitotic exit. (C) 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:2720 / 2726
页数:7
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