| Project/Area Number |
15K11093
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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 |
Pathobiological dentistry/Dental radiology
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| Research Institution | Matsumoto Dental University |
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Principal Investigator |
Hiraga Toru 松本歯科大学, 歯学部, 教授 (70322170)
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| Co-Investigator(Kenkyū-buntansha) |
細矢 明宏 北海道医療大学, 歯学部, 准教授 (70350824)
二宮 禎 日本大学, 歯学部, 准教授 (00360222)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | がん / 骨転移 / がん幹細胞 / EpCAM |
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| Outline of Final Research Achievements |
In the current study, we examined the roles of epithelial cell adhesion molecule (EpCAM) in the development of cancer bone metastasis. EpCAM-negative (EpCAMneg) and EpCAM-positive (EpCAMpos) populations isolated from cancer cell lines exhibited mesenchymal and epithelial phenotypes, respectively. Flow cytometric analysis revealed that EpCAMpos, but not EpCAMneg, cells possessed self-renewal and differentiation potentials. Tumorsphere formation in vitro and tumorigenicity in the mammary fat pad of mice were significantly greater in EpCAMpos cells than in EpCAMneg cells. Furthermore, the development of bone metastases was markedly increased in mice inoculated with EpCAMpos cells. These results suggest that the expression of EpCAM in cancer cells is associated with cancer stem-like phenotypes, which contribute to the promotion of bone metastases by enhancing tumorigenicity.
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