| Project/Area Number |
22657045
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
Cell biology
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| Research Institution | Hokkaido University |
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Principal Investigator |
HASHIMOTO Sigeru 北海道大学, 大学院・医学研究科, 准教授 (50311303)
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| Project Period (FY) |
2010 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥3,360,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2010: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | 癌浸潤 / 癌幹細胞 / マクロファージ / 乳癌細胞 / 細胞間融合 / Arf6 / GEP100 / AMAP1 |
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| Research Abstract |
In 1911, Otto Aichel postulated the concept of cell fusion as a mechanism of tumor malignancy. Recently, there are a lot of clinical and experimental discoveries of cell fusion as one of the driving forces of tumor progression. However, its molecular mechanisms remain to be elucidated. We have previously shown that GEP100-Arf6-AMAP1 signaling pathway contributes to the acquisition of invasiveness of some breast cancer cells. Here, we found that Arf6 and GEP100 were involved in the regulation of cell-cell fusion between highly invasive breast cancer cells, or bone marrow-derived cells.
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