| Project/Area Number |
12671214
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Digestive surgery
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| Research Institution | 福井医科大学 |
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Principal Investigator |
ISHIDA Makoto Fukui Medical University, First Department of Surgery, Assistant, 医学部, 教授 (10174608)
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| Co-Investigator(Kenkyū-buntansha) |
石田 誠 福井医科大学, 医学部, 助手 (00311689)
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| Project Period (FY) |
2000 – 2001
|
| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 2001: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2000: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | Aurora2 / gl-rine / threonine protein / ubiquitination / APC-ubiquitin-proteasome pathway / スレオニンキナーゼ / Aurora2 / Colorectal Cancer |
|---|
| Research Abstract |
Human Aurora2 was originally identified by its close homology to yeast IPL1 and fly aurora, which are key regulators of chromosome segregation and a cell cycle regulated serine/threonine protein kinase which is overexpressed in many tumor cell lines. We analyzed 100 colorectal cancer specimens for the expresssion of Aurora2 gene. The overexpression of Aurora2 gene was 62 % in primary colorectal cancers. Furthermore, we demonstrated that the Aurora2 protein is degraded rapidly after G2/M phase release in mammalian cells, (a half-life of approximately 2 h). The treatment of the cells with proteasome inhibitors blocks Aurora2 degradation. Aurora2 is polyubiquitinated in vivo and in vitro using anaphase-promoting complex (APC). These results demonstrate that Aurora2 protein js turned over through the APC-ubiquitin-proteasome pathway.
We hope that the regulation of APC-ubiquitin-proteasome pathway may be useful for tumor dormancy therapy.
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