2018 Fiscal Year Final Research Report
Development of a therapeutic agent for oral cancer applying a naturally derived component with EGFR signal inhibitory effect.
| Project/Area Number |
16K11707
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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 |
MAEHATA YOJIRO 神奈川歯科大学, 大学院歯学研究科, 特任講師 (80410009)
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| Co-Investigator(Kenkyū-buntansha) |
畑 隆一郎 神奈川歯科大学, 大学院歯学研究科, 特任教授 (10014276)
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Keywords | 口腔癌 / CXCL14/BRAK / 癌幹細胞 |
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| Outline of Final Research Achievements |
At the beginning of this study, we planned to find regulation mechanisms of CXCL14/BRAK by fatty acid acetogenins in head and neck squamous cell carcinoma cell (HSC-3), but we could not find conditions that regulates BRAK expression in the cells. Therefore, the research program has been changed to investigate effect of BRAK on the gene expression of oral carcinoma cells.Because we found that BRAK transgenic mice suppressed various types of cancer, we examined the effects BRAK on the stem cell factors and cancer stem cell factor expression using HSC-3 cells and BRAK over expressed HSC-3 cells and BRAK knock downed cells. As a result, we found that BRAK over expression suppresses tumor progression, together with the decreased expression in stem cell factors and cancer stem cell factor. These results indicate that BRAK may regulate tumor progression through regulation of cancer stem cell factor expression. These data are useful for future development of cancer progression by use of BRAK.
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| Free Research Field |
歯科薬理学
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| Academic Significance and Societal Importance of the Research Achievements |
ヒトの癌組織中には，自己複製能，多分化能および無制限な増殖能を併せ持つ癌幹細胞が存在することが報告されている。また，癌幹細胞は癌の再発, 転移および薬剤耐性の獲得に関与する事が知られている。口腔癌においても，癌幹細胞マーカー（CD44V）陽性の口腔癌幹細胞の存在が報告されている。本研究結果から，口腔癌において，発癌，癌細胞増殖および転移を抑制する多段階癌抑制因子であるCXCL14/BRAKの発現上昇により，CD44Vおよび幹細胞因子NANOG，KLF4の発現が抑制されることが示された。口腔癌におけるBRAKの発現を上昇させる分子の検索は，口腔癌の分子標的治療に有用であると考えられる。
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