| Project/Area Number |
25462686
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Otorhinolaryngology
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| Research Institution | Kyushu University |
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Principal Investigator |
Toh Satoshi 九州大学, 医学(系)研究科(研究院), 研究員 (20380397)
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| Co-Investigator(Kenkyū-buntansha) |
NAKASHIMA TORAHIKO 九州大学, 医学研究院, 准教授 (00284505)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 上皮細胞増殖因子受容体 / 細胞膜脂質構造 / Srcファミリー / 上皮増殖因子受容体 / 内在化 / 脂質 |
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| Outline of Final Research Achievements |
EGFR, which is expressing in various carcinoma cells, plays critical roles of proliferation, invasion and metastasis. Some molecular targeting drugs against EGFR are already applied for cancer patients. In this study, we investigated a mechanism of c-src activation, which might cause internalization of EGFR.
EGCG, a constituent of green tea, cause EGFR internalization. This is inhibited by src family kinase inhibitors. Using YCU-H891 cells (head and neck cancer origin), we conducted a EGFR internalization study and found that EGCG induced EGFR internalization was inhibited 2 hydroxypalmitate (N-terminal palmitoylation inhibitor) and G2A-c-src transfection (acting as dominant negative manner about N-terminal palmitoylation of c-src) . We also found that EGCG preferentially activate c-src among SFKs. As EGCG and other polyphenol compounds alter lipid organization of membrane, anchoring and localization of c-src might be critical for its activation by EGCG.
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