期刊
CANCER LETTERS
卷 275, 期 1, 页码 77-85出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.canlet.2008.10.011
关键词
Cyclin B1; Aurora-A; Cell cycle; Protein stability; Carcinogenesis
类别
资金
- 973 National Key Fundamental Research Program of China [2002 CB5131 01]
- National Natural Science Foundation of China [30730046, 30721001]
The mitotic regulator Aurora-A is an oncogenic protein that is over-expressed in many types of human tumors. However, the underlying mechanism through which Aurora-A promotes tumorigenesis remains unclear. Here, we show that overexpression of Aurora-A causes an elevation of Cyclin B1 expression. Cyclin B1 degradation is delayed in Aurora-A over-expressing cells, which depends on Aurora-A kinase activity. In contrast, Aurora-A RNAi enhances Cyclin B1 degradation. Furthermore, we found that Aurora-A interacts with Cyclin B1, and that Aurora-A overexpression reduces the interaction of Cyclin B1 with APC subunits. In human esophageal squamous cell carcinomas (ESCC), overexpression of Aurora-A was correlated with deregulated expression of Cyclin B1. Taken together, these findings suggest that overexpression of Aurora-A may stabilize Cyclin B1 through inhibiting its degradation. These results provide new insight into the mechanism of how deregulated Aurora-A contributes to genomic instability and carcinogenesis. (C) 2008 Elsevier Ireland Ltd. All rights reserved.
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