| Project/Area Number |
16K20579
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Surgical dentistry
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| Research Institution | Okayama University |
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Principal Investigator |
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| Research Collaborator |
SASAKI Akira 岡山大学, 大学院医歯薬学総合研究科, 教授 (00170663)
SHIMO Tsuyoshi 北海道医療大学, 歯学部, 教授 (40362991)
KISHIMOTO Koji 岡山大学, 大学院医歯薬学総合研究科, 助教 (40243480)
MURASE Yurika 岡山大学, 大学病院, 医員 (70803708)
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | PRL-3 / 口腔扁平上皮癌 / 浸潤 |
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| Outline of Final Research Achievements |
This study assessed the function of PRL-3 in the progression of oral squamous cell carcinoma. In human oral squamous cell carcinoma cell lines, PRL-3 showed an expression pattern similar to that of E-cadherin which disappears in the course of epithelial-mesenchymal transition (EMT). E-cadherin was also highly expressed in the most invasive part of the oral squamous cell carcinoma tissue in which PRL-3 is highly expressed. In addition, the expression of PRL-3 was low in gingival squamous cell carcinoma tissues with jaw bone invasion. On the contrary, PRL-3 and E-cadherin were both highly expressed in the gingival squamous cell carcinoma tissue without the jaw bone invasion. These results demonstrated that PRL-3 has a function of suppressing EMT via E-cadherin and suppress the invasion of oral squamous cell carcinoma.
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| Academic Significance and Societal Importance of the Research Achievements |
学術的意義：本研究から、PRL-3はE-cadherinを介してEMTを抑制し、口腔扁平上皮癌の浸潤を抑制する可能性が推察された。また、PRL-3は顎骨浸潤も抑制する可能性が示唆された。
社会的意義：本研究から、PRL-3が口腔扁平上皮癌の浸潤の早期診断マーカーになることが期待でき、PRL-3を分子標的とした浸潤抑制薬開発への貢献が期待できる。
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