2021 Fiscal Year Final Research Report
The elucidation of the pathophysiology of gingival overgrowth.
| Project/Area Number |
18K09578
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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 57030:Conservative dentistry-related
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| Research Institution | Kyushu University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
西村 英紀 九州大学, 歯学研究院, 教授 (80208222)
岩下 未咲 九州大学, 歯学研究院, 助教 (80611326)
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| Project Period (FY) |
2018-04-01 – 2022-03-31
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| Keywords | 歯肉増殖症 / SPOCK1 |
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| Outline of Final Research Achievements |
SPOCK1 is an extracellular proteoglycan that induces epithelial to mesenchymal transition (EMT) in several cancer cell lines and exhibits protease-inhibitory activity. However, the role of SPOCK1 in non-cancerous diseases such as DIGO has not been well-addressed. We demonstrated that the expression of SPOCK1, TGF-β1, and MMP-9 in calcium channel blocker-induced gingival overgrowth is higher than that in non-overgrowth tissues. Transgenic mice overexpressing Spock1 developed obvious gingival-overgrowth and fibrosis phenotypes, and positively correlated with EMT-like changes. Furthermore, in vitro data indicated a tri-directional interaction between SPOCK1, TGF-β1, and MMP-9 that led to gingival overgrowth. Our study shows that SPOCK1 up-regulation in a noncancerous disease and SPOCK1-induced EMT in gingival overgrowth occurs via cooperation and crosstalk between several potential signaling pathways.
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| Free Research Field |
歯周病学
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| Academic Significance and Societal Importance of the Research Achievements |
これまでに癌領域におけるSPOCK1の機能に関しては、比較的多くの報告があるものの、非癌性疾患においてはほとんど報告されていなかった。本研究において、非癌性疾患におけるSPOCK1のアップレギュレーションと、歯肉増殖症におけるSPOCK1によって誘発されるEMTが、いくつかの潜在的なシグナ ル伝達経路間のクロストークを介して発生sすることを明らかにした点に意義がある。SPOCK1は歯肉増殖症の新しい治療標的となり得る可能性を示し、その発現は癌性病変におけるEMT誘導の潜在的なリスクであると考えられ、今後の癌領域研究においてメカニズム解明の一助となる可能性がある。
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