| Project/Area Number |
23591978
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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 |
Digestive surgery
|
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| Research Institution | Chiba Cancer Center (Research Institute) |
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Principal Investigator |
SOUDA Hiroaki 千葉県がんセンター(研究所), 医療局・消化器外科, 研究員 (90261940)
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| Co-Investigator(Kenkyū-buntansha) |
SHIMOZATO Osamu 千葉県がんセンター(研究所), 発がん研究グループ, 上席研究員 (30344063)
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| Project Period (FY) |
2011 – 2013
|
| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 癌幹細胞 / CD133 / 活性酸素種 / 大腸がん / 癌性幹細胞 / ＣＤ１３３ / ROS産生 |
|---|
| Research Abstract |
As tyrosine residues of CD133 are phosphorylated in human colon cancer-derived cells, we sought for its functional significance in colon carcinogenesis. Consequently, we found that CD133 phosphorylation enhances xenograft tumor growth and sphere formation of colon cancer-derived cells. Additionally, we identified receptor-type protein tyrosine phosphatase  (PTPRK), a novel binding-partner of CD133, which dephosphorylates CD133 and thereby suppressing CD133-mediated oncogenic function. Indeed, lower PTPRK expression significantly correlated to the poor prognosis of colon cancer patients with higher expression of CD133. Thus, our present findings strongly suggest that inhibition of CD133 phosphorylation is a crucial issue for improving colon cancer treatment in future.
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