2023 Fiscal Year Final Research Report
Anti-tumor Effect of Nicotinic Acid Activation on Canine Mastocytoma through GPER and Immunological Analysis of Tumor Microenvironment
| Project/Area Number |
21K05927
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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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| Review Section |
Basic Section 42020:Veterinary medical science-related
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| Research Institution | Azabu University |
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Principal Investigator |
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| Project Period (FY) |
2021-04-01 – 2024-03-31
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| Keywords | イヌ肥満細胞腫 / KIT非依存性 / 肥満細胞腫マウスモデル / ナイアシン / ニコチン酸 / ニコチンアミド / GPER / 抗腫瘍作用 |
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| Outline of Final Research Achievements |
In the treatment of cancer in dogs, especially in elderly dogs, drug administration is often necessary, considering the burden of surgical procedures. Therefore, there is a demand for therapeutic agents with low drug resistance and fewer side effects. In previous studies conducted by us, it was found that the administration of niacin induced cell death in canine mastocytoma cells. Although the antitumor effects of niacin have been previously reported, only the receptor GP109A has been highlighted as mediating its action. This study aimed to uncover a new aspect of the antitumor mechanism of niacin by investigating the involvement of not only GPR109A but also GPER.
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| Free Research Field |
獣医学
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| Academic Significance and Societal Importance of the Research Achievements |
報告者はこれまでに膜型エストロゲン受容体GPERの選択的アゴニストがマウスやイヌの肥満細胞腫細胞に細胞死を誘導することを見出した．さらにナイアシン（ニコチン酸，ニコチンアミド）がGPERを介して細胞内にシグナルを伝えることが報告されたため，ナイアシンによる抗腫瘍効果について検討したところ，ナイアシンが肥満細胞腫細胞の細胞死を誘導することを見出した．さらにマウス肥満細胞腫モデル系においてナイアシンの投与は腫瘍の増大を抑制しリンパ球の浸潤を促進することが示唆された．GPERの選択的アゴニストに比べナイアシンはコストが低く，さらに詳細な解析・検討を行うことであらたな治療法への提案に繋がると期待される
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