KLF-dependent cell differentiation- and EMT-inducing factor and suppression of oral carcinoma progression
Project/Area Number |
26462859
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Pathobiological dentistry/Dental radiology
|
Research Institution | The Nippon Dental University |
Principal Investigator |
Imai Kazushi 日本歯科大学, 生命歯学部, 教授 (10328859)
|
Co-Investigator(Kenkyū-buntansha) |
須藤 遙 日本歯科大学, 生命歯学部, 講師 (20372980)
千葉 忠成 日本歯科大学, 生命歯学部, 准教授 (60350138)
|
Co-Investigator(Renkei-kenkyūsha) |
MIHARA Nozomi 日本歯科大学, 生命歯学部, 助教 (00803264)
|
Project Period (FY) |
2014-04-01 – 2018-03-31
|
Project Status |
Completed (Fiscal Year 2017)
|
Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2017: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2016: ¥520,000 (Direct Cost: ¥400,000、Indirect Cost: ¥120,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
|
Keywords | 口腔癌 / KLF / プロモーター / KLF5 / 口腔癌細胞 / サイレンサー / Sp3 / 転写因子 / Sp1 |
Outline of Final Research Achievements |
Kruppel-like factor (KLF) plays a critical role in epithelial tissue development and homeostasis. Expression balance of KLF4 and KLF5 is considered to regulate carcinoma cell phenotypes and carcinoma progression. However, very little is known about a role KLF4/5 in oral carcinomas. This study demonstrated that KLF4/5 regulate differentiation and dedifferentiation of oral carcinoma cells and that expression of KLF4 are suppressed by hypermethylation of the gene promoter. In regard to KLF5 expression, a region from +145 to +330 act as a minimal essential region and Sp3 binding to GC box was a indispensable event.
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Report
(5 results)
Research Products
(9 results)