| Project/Area Number |
20791015
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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 |
Cerebral neurosurgery
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| Research Institution | Oita University |
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Principal Investigator |
MORISHIGE Masaki Oita University, 医学部, 助教 (60381050)
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| Project Period (FY) |
2008 – 2009
|
| Project Status |
Completed (Fiscal Year 2009)
|
| Budget Amount *help |
¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2009: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2008: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 脳腫瘍 / 浸潤 / 分子標的 / 神経膠芽腫 / 増殖因子 |
|---|
| Research Abstract |
Glioblastoma multiforme (GBM) is the most invasive form in gliomas and extremely refractory to therapy. Invasive phenotypes are considered to be a principal factor of poor prognosis. An investigation of the molecules regulating invasion will thus contribute to the GBM treatment. We have previously shown that Arf6 plays an important role in the invasive activities of human breast cancer, and also AMAP1, an effector of GTP-Arf6, is involved in the invasive mechanism by binding Cortactin and Paxillin in breast cancer. We here found that AMAP1 is highly expressed in primary human gliomas, and blockage this complex formation, by using of cell-permeable proline peptide derived from the AMAP1 inhibits GBM invasion in vitro. Our results indicate that Arf6 and its regulator are the major components of cancer invasive activities, and propose novel pharmaceutical targets for prevention GBM invasion.
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