2022 Fiscal Year Final Research Report
Suppression of oral cancer metastasis by inhibition of selective autophagy targeting cell adhesion molecules
| Project/Area Number |
19K10310
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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 57060:Surgical dentistry-related
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| Research Institution | Hiroshima University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
岡本 哲治 東亜大学, その他の研究科, 教授 (00169153)
新谷 智章 広島大学, 病院(歯), 講師 (90403518)
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| Project Period (FY) |
2019-04-01 – 2023-03-31
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| Keywords | 口腔癌 / 浸潤・転移 / オートファジー / インテグリン / p62 |
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| Outline of Final Research Achievements |
Integrin αv subunit forms a complex with p62 in squamous cell carcinoma cells, resulting in the degradation of αv subunit via selective autophagy. It has been shown the possibility that αv subunit dimerized with β3, β5, β6 or β8 subunit is resistant to lysosomal degradation and stably expressed as αvβ3, αvβ5, αvβ6 or αvβ8 that regulates cellular functions. Integrin αvβ5 is involved in the suppression of tumorigenic potential of squamous cell carcinoma cells while αvβ1, αvβ3 and αvβ6 are involved in the enhancement of tumorigenic potential, suggesting that integrin αv subfamily such as αvβ1, αvβ3, αvβ5, αvβ6 could serve as a therapeutic target to prevent the progression of squamous cell carcinomas including oral cancer.
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| Free Research Field |
口腔外科
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| Academic Significance and Societal Importance of the Research Achievements |
本研究で明らかになった選択的オートファジーによるインテグリンαv分子の分解機構の解明は，組織分化や器官発生のメカニズム，細胞の癌化や癌の進展機構を理解する上で重要な知見をもたらすだけではなく，従来の癌治療にかわる新しい口腔癌治療法開発の一助になることが期待される．さらに,上記に示されたオートーファジー系による蛋白翻訳後修飾や分解機構は，異常タンパク質の細胞内への蓄積を特徴とするアルツハイマー病，パーキンソン病，ポリグルタミン病，筋萎縮性側索硬化症などの神経変性疾患の病態解明や治療法開発に関する研究を行う上で有用な知見となるものと期待できる．
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