| Project/Area Number |
26463014
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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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| Research Field |
Surgical dentistry
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| Research Institution | Kyushu University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
豊嶋 健史 九州大学, 歯学研究院, 共同研究員 (20546569)
中村 誠司 九州大学, 歯学研究院, 教授 (60189040)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 浸潤 / 転移 / 口腔癌 / 上皮間葉転換 / ZEB1 / ZEB2 / deltaNp63 / 口腔扁平上皮癌 / ZEBファミリー / ΔNp63 / miR205 / 上皮-間葉転換 |
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| Outline of Final Research Achievements |
Previously, microRNA (miR) microarray analyses were performed to identify the responsible gene for epithelial-mesenchymal transition ( EMT）mediated by ΔNp63β in oral squamous cell carcinoma (OSCC). As the results, we focused on miR-205 that is up-regulated by ΔNp63β-forced expression. The inhibitor for miR-205 was thus added into the culture supernatant of OSCC cells strongly expressingΔNp63β. And then, expression of zinc finger E-box binding homeobox (ZEB)1 and ZEB2 was up-regulated, epithelial markers including cytokeratin 19 and E-cadherin were also down-regulated, mesenchymal markers were up-regulated. Furthermore, capacities of invasion and migration were enhanced by the treatment of inhibitor for miR-205. These results showed tumor-suppressive roles of ΔNp63β and miR-205 by inhibiting EMT thorough modulating ZEB1 and ZEB2 expressions in OSCC.
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