| Project/Area Number |
17K11859
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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 |
Surgical dentistry
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| Research Institution | Kanagawa Dental College |
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Principal Investigator |
Suzuki Kenji 神奈川歯科大学, 大学院歯学研究科, 講師 (80350536)
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| Co-Investigator(Kenkyū-buntansha) |
小澤 重幸 神奈川歯科大学, 大学院歯学研究科, 講師 (40434394)
小林 優 神奈川歯科大学, 大学院歯学研究科, 教授 (00162024)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2019: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 頭頚部扁平上皮癌 / CXCL14 / GPRC5b / p53 / p５３ / SCC / 口腔外科学一般 |
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| Outline of Final Research Achievements |
We found that the expression of the chemokine ligand 14 gene (CXCL14) increases upon culturing a head and neck squamous cell carcinoma cell line in a sugar-free medium, followed by supplementation with sugar. These findings suggest that CXCL14 might be a sugar-sensitizing gene and could be related to the recently reported GPRC5b gene, which encodes a G protein-coupled receptor family C protein. Upon further examination, it was found that the addition of sugar increased GPRC5b expression, as seen with CXCL14. Moreover, mechanistic analysis of GPRC5b revealed that its metabolism is mediated by malonyl CoA. There have been no prior reports on the effect on the metabolism of GPRC5b, making this the first elucidative attempt to study this role.
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| Academic Significance and Societal Importance of the Research Achievements |
癌は細胞の増殖を促す遺伝子とそれにブレーキをかける遺伝子に異常が生じることで発生すると考えられている。p53は代表的ながん抑制遺伝子であるが、p53の癌細胞に対する増悪化メカニズムに、細胞のエネルギーセンサーであるGPRC5bが関与するのではないかと考え研究を行った。その結果、癌細胞が低栄養の環境下に置かれるとGPRC5bが活性化し、更に癌細胞の自然死を誘発する酵素の代謝が抑制されることで、癌細胞の自然死が回避されるのではないかいう新しい知見を得ることができた。
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