| Project/Area Number |
26640088
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Tumor biology
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| Research Institution | Nagoya City University |
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Principal Investigator |
Kondo Yutaka 名古屋市立大学, 医学(系)研究科(研究院), 教授 (00419897)
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| Co-Investigator(Renkei-kenkyūsha) |
SHINJO Keiko 名古屋市立大学, 大学院医学研究科, 助教 (40641618)
NATSUME Atsushi 名古屋大学, 大学院医学研究科, 准教授 (30362255)
SUZUKI Takayoshi 京都府立医科大学, 大学院医学研究科, 教授 (90372838)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | グリオブラストーマ / エピジェネティクス / 治療 / 膠芽腫 / エピゲノム / 癌治療 / ヒストン修飾 / 遺伝子変異 |
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| Outline of Final Research Achievements |
In the current project, using mouse model (Tp53 and Nf1 loss), which spontaneously develops proneural GBM, we found that a certain specific gene locus is commonly (100%) amplified in multiple mice (n=5). In addition, although HMT-1 is not located in the amplified locus, it was overexpressed from early stage of gliomagenesis in this model. Intriguingly, among the genes located in commonly amplified locus, we identified HMT-2, which forms aberrant complex with HMT-1 in the tumor cells. Inhibition of HMT-1 and/or HMT-2 by a small molecules or siRNA system efficiently suppressed the tumor growth both in vitro and in vivo. Our data indicate that targeting these molecules (HMT-1 and HMT-2) may be a novel and potent therapeutic strategy for GBMs, especially proneural subtype.
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