| Literature DB >> 19028417 |
Lili Qin1, Tong Tong, Yongmei Song, Liyan Xue, Feiyue Fan, Qimin Zhan.
Abstract
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.Entities:
Mesh：
Substances：
Year: 2008 PMID： 19028417 DOI： 10.1016/j.canlet.2008.10.011
Source DB: PubMed Journal: Cancer Lett ISSN： 0304-3835 Impact factor: 8.679