2019 Fiscal Year Final Research Report
Role and regulatory mechanisms of Semaphorin 4D in bone invasion of oral cancer.
Project/Area Number |
17K11836
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Surgical dentistry
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Research Institution | Okayama University |
Principal Investigator |
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Co-Investigator(Kenkyū-buntansha) |
佐々木 朗 岡山大学, 医歯薬学総合研究科, 教授 (00170663)
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Project Period (FY) |
2017-04-01 – 2020-03-31
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Keywords | Semaphorin 4D / 口腔癌骨浸潤 |
Outline of Final Research Achievements |
In the bone microenvironment, axon guidance molecule Semaphorin 4D (Sema4D) that was secreted by osteoclasts, suppressed bone formation. Sema4D was also identified in many cancer cells and plays a role in tumor growth. This research demonstrated the role of Sema4D in bone invasion of oral cancer. Sema4D that was produced by oral cancer cells, increased cancer cell activity in an autocrine manner. Sema4D also regulated the expression of RANKL in osteoblasts, and which stimulated osteoclastgenesis and bone invasion of oral cancer cells. IGF-I that was released from destructed bone tissue, regulated Sema4D expression and increased further tumor growth and bone invasion.
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Free Research Field |
口腔外科
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Academic Significance and Societal Importance of the Research Achievements |
本研究は,口腔癌細胞の産生するSema4Dが口腔癌細胞の増殖と破骨細胞形成を促進し,骨浸潤を促進していることを明らかにした.さらに口腔癌細胞のSema4D発現を制御しているのは,破壊された骨組織から遊離されたIGF-Iであることを突き止めた.本研究を発展させ抗Sema4D 療法が臨床応用できれば,癌細胞および破骨細胞の両方を標的とした新規治療法の候補となると考えられた.
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