| Project/Area Number |
25460062
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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 |
Biological pharmacy
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| Research Institution | Tokyo University of Agriculture and Technology |
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Principal Investigator |
MIYAURA CHISATO 東京農工大学, 工学(系)研究科(研究院), 教授 (20138382)
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| Co-Investigator(Kenkyū-buntansha) |
INADA MASAKI 東京農工大学, 大学院工学研究院, 准教授 (80401454)
HIRATA MICHIKO 東京農工大学, 大学院工学研究院, 講師 (40544060)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 乳がん / 骨転移 / 骨吸収 / プロスタグランジンE / 血管新生 / 固形腫瘍 / イメージング解析 |
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| Outline of Final Research Achievements |
Bone metastasis is a frequent occurrence in breast cancer patients, but little is known about the role of prostaglandin E (PGE) in the cancer. We established the model for bone metastasis of breast cancer in mice. When breast cancer cell (4T1) was injected in to tibia, severe bone resorption was detected in the metastasis area by micro-CT analysis. Bone resorption induced by PGE is mainly regulated by the signaling via EP4 receptor, one of the PGE receptor subtypes. The bone metastasis of breast cancer with increased bone resorption was abrogated by EP4 receptor antagonist in vivo. The cell-cell interaction with 4T1 induced PGE production in osteoblasts, suggesting that PGE-EP4 signaling may be critical for bone destruction in bone metastasis of breast cancer. Metastasis of prostate cancer PC-3 was detected in vivo, and both metastasis into various tissues and bone metastasis was clearly suppressed by the treatment with EP4 antagonist in mice.
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