| Project/Area Number |
25861742
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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 |
Morphological basic dentistry
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| Research Institution | Kawasaki Medical School |
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Principal Investigator |
Katase Naoki 川崎医科大学, 医学部, 助教 (30566071)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 頭頸部扁平上皮癌 / 扁平上皮癌 / DKK3 / がん抑制遺伝子 / 遺伝子機能解析 / 口腔扁平上皮癌 / Wnt signaling / 機能解析 / 細胞増殖 / 浸潤 / 転移 / 強制発現 / western blotting / Real time PCR / ELISA / Transfection |
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| Outline of Final Research Achievements |
In this research project, functional analyses on DKK3 gene were performed in head and neck squamous cell carcinoma (HNSCC). Although DKK3 is known as tumor suppressor of which expression is reduced in many kinds of malignancies, its expression is specifically high in HNSCC. In the present research, DKK3 overexpression (DKK3-OE) and DKK3 stable knockdown (DKK3-KD) were established, and detailed investigation was done on DKK3-OE model. DKK3-OE resulted in increased cellular proliferation, migration and invasion. Moreover, DKK3-OE cells showed increased tumor volume in nude mice xenograft model. To explain these results, influence of DKK3-OE on Wnt/β-catenin signal was investigated. However, TCF activity that will be increased by Wnt/β-catenin signal was not increased, although Wnt target gene expression was elevated. The results imply that DKK3 may exert oncogenic function via certain signal other than Wnt/β-catenin signal, specifically in HNSCC.
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