| Project/Area Number |
23501271
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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 |
Tumor biology
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| Research Institution | Tokyo University of Science |
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Principal Investigator |
TASHIRO Fumio 東京理科大学, 基礎工学部, 教授 (70089332)
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| Co-Investigator(Kenkyū-buntansha) |
AKIYAMA Hirotada 東京理科大学, 基礎工学部生物工学科, 助教 (40400254)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2012: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2011: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
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| Keywords | がん制御因子 / 14-3-3 / FBI1/Akinin2 / 転移 / がん促進遺伝子 / 癌幹細胞 / 上皮間葉転換 / がん抑制遺伝子 / 14-3-3ファミリータンパク質 |
|---|
| Research Abstract |
We previously demonstrated that 14-3-3beta protein promotes cell growth and tumorigenicity of rat K2 hepatocellular carcinoma cells. We identified FBI1/Akirin2 as a binding partner of 14-3-3beta and showed that the complex of these proteins promotes tumorigenicity and metastasis of K2 cells. Based on microarray expression analysis, BCAM and SPARC were identified as the downregulated target genes of the oncogenic 14-3-3beta-FBI1/Akirin2 complex. BCAM and SPARC are suppressive oncoprotein, and that FBI1/Akirin2 is involved in tumorigenicity and metastasis of hepatoma through the downregulation of suppressive oncogenes. Furthermore, we demonstrated that FBI1/Akirin2 performs an oncogenic function in LLC1 Lewis lung carcinoma cells. Although further investigation is required, these results suggest that FBI1/Akirin2 may perform an universal oncogenic function in various cancers.
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