| Project/Area Number |
21790380
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Experimental pathology
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| Research Institution | Kyoto University |
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Principal Investigator |
WATANABE Akira Kyoto University, iPS細胞研究所, 特定拠点助教 (60506765)
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| Co-Investigator(Renkei-kenkyūsha) |
ABURATANI Hiroyuki 東京大学, 先端科学技術研究センター, 教授 (10202657)
MIYAZONO Kohei 東京大学, 医学部, 教授/学部長 (90209908)
FUKAYAMA Masashi 東京大学, 医学部, 教授 (70281293)
SAITO Nobuhito 東京大学, 医学部, 教授 (60262002)
MUKASA Akitake 東京大学, 医学部, 特任講師 (90463869)
YAMADA Yasuhiro 京都大学, iPS細胞研究所, 特定拠点教授 (70313872)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2010: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2009: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 癌幹細胞 / DACH1 / 脳腫瘍 / 分子生物学 / 癌抑制遺伝子 |
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| Research Abstract |
Loss or reduction in function of tumor suppressor genes contributes to tumorigenesis. Here, by allelic DNA copy number analysis, we report homozygous deletion in glioblastoma multiformes (GBMs) at chromosome 13q21, where DACH1 gene is located. We found decreased cell proliferation by forced expression of DACH1. Exogenous bFGF, a target gene of DACH1, rescues spheroid-forming activity and tumorigenicity of the U87-DACH1-high cells, suggesting that loss of DACH1 increases the number of tumor-initiating cells through transcriptional repression of bFGF. These results illustrate that DACH1 is a novel tumor suppressor, which does not only suppress growth of tumor cells but also regulates bFGF-mediated tumor-initiating activity of glioma cells.
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