| Project/Area Number |
17K16510
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
General surgery
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| Research Institution | Ehime University |
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Principal Investigator |
Murakami Akari 愛媛大学, 医学部附属病院, 助教 (60722593)
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| Research Collaborator |
Maekawa Masashi
Kawai Katsuhisa
Nakayama Jun
Araki Nobukazu
Semba Kentaro
Taguchi Tomohiko
Kamei Yoshiaki
Takada Yasutsugu
Higashiyama Shigeki
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| Project Period (FY) |
2017-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2018: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2017: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 乳癌 / CUL3 / 細胞特性 / HER2陽性乳癌 / 乳癌細胞特性解析 / 乳癌細胞 / 細胞膜形態 / 幹細胞 / ユビキチンリガーゼ |
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| Outline of Final Research Achievements |
Human breast cancer can be classified by gene expression into four or five subtypes, and the treatment plans are decided based on the subtypes. From this standpoint, it is important to elucidate molecular mechanisms of the determination of breast cancer characteristics, which could lead to the development of novel therapy for breast cancers. In this research proposal, we focused on a ubiquitin E3 scaffold protein, cullin-3 (CUL3), and found that CUL3 is essential for Rac1 activation and cell proliferation specifically in HER2-positive breast cancer cells.
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| Academic Significance and Societal Importance of the Research Achievements |
HER2陽性乳癌細胞で予後を規定するRac1の新しい活性化機構として、CUL3/KCTD10/RhoB軸の同定に成功した。今後は、CUL3/KCTD10依存的に活性化されるRac1の詳細な生理機能の解明が期待される。
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