Aurora-A interacts with Cyclin B1 and enhances its stability
| Autor: | Lili Qin, Fei-Yue Fan, Liyan Xue, Qimin Zhan, Yongmei Song, Tong Tong |
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| Rok vydání: | 2009 |
| Předmět: |
Cancer Research
Cyclin E Esophageal Neoplasms Cyclin D Cyclin A Cyclin B Cell Cycle Proteins macromolecular substances Protein Serine-Threonine Kinases Gene Expression Regulation Enzymologic Cyclin D1 Aurora Kinases Cell Line Tumor Humans Cyclin B1 Oligonucleotide Array Sequence Analysis biology Ubiquitin Chemistry Cell Cycle Cell cycle Immunohistochemistry Cell biology Gene Expression Regulation Neoplastic enzymes and coenzymes (carbohydrates) Oncology embryonic structures Carcinoma Squamous Cell biology.protein RNA Interference biological phenomena cell phenomena and immunity Cyclin A2 |
| Zdroj: | Cancer Letters. 275:77-85 |
| ISSN: | 0304-3835 |
| DOI: | 10.1016/j.canlet.2008.10.011 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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