| Project/Area Number |
17K19748
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| Research Category |
Grant-in-Aid for Challenging Research (Exploratory)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Oral Science and related fields
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| Research Institution | Niigata University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
山崎 学 新潟大学, 医歯学系, 助教 (10547516)
三上 剛和 新潟大学, 医歯学系, 准教授 (80434075)
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| Research Collaborator |
Amaya Yoshihiro
Harada Fumiko
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| Project Period (FY) |
2017-06-30 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥6,370,000 (Direct Cost: ¥4,900,000、Indirect Cost: ¥1,470,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2017: ¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
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| Keywords | AMPK / 口腔癌 / 扁平上皮癌 / GABA / シグナル伝達 / 口腔がん / キナーゼ / 神経伝達物質 / 口腔扁平上皮癌 / GABAB受容体 / AMPキナーゼ / 蛋白質 / 癌 |
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| Outline of Final Research Achievements |
We examined the anticancer effect of cellular energy sensor AMPK and inhibitory neurotransmitter receptor GABAB receptor and their functional crosstalk in oral cancer cells. We found that the structure of GABAB receptors are different from that of neuronal GABAB receptors and their activation did not induce anti-cancer effect. On the other hand, AMPK activation strongly suppressed the cancer proliferation. Therefore, in oral cancer, AMPK downstream signaling maybe a good target for novel drug development.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究により、他の組織のがんで報告されていたGABAB受容体の活性化によるがん抑制効果が口腔がんでは発揮されないことが明らかとなった。一方、AMPKやその下流分子の活性化が効果的な癌抑制効果を生み出すことも明らかとなり、今後これらを標的とした研究が、新規抗がん剤の開発などに繋がる可能性がある。
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