| Project/Area Number |
23701071
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Tumor biology
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| Research Institution | Research Institute, Osaka Medical Center for Cancer and Cardiovascular Disaeses |
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Principal Investigator |
OKAMOTO Miki 地方独立行政法人大阪府立病院機構大阪府立成人病センター(研究所), 研究所, 研究員 (20332455)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2012: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | 細胞接着 / 運動 / 発がん / 腸上皮細胞 / 細胞骨格リモデリング / がん / 細胞運動 |
|---|
| Research Abstract |
Afadin interacts with the cytoplasmic region of nectins, immunoglobulin-like cell adhesion molecules at adherens junctions, links them to the actin cytoskeleton, and regulates cytoskeletal remodeling. However, it remains unknown whether afadin plays roles in tumorigenesis and tumor progression. Previously we reported that in afadin intestine-specific deficient mice, the paracellular permeability in the intestinal mucosa increased and susceptibility to the tissue destruction induced by dextran sulfate sodium enhanced. Here we treated the mice with azoxymethan and dextran sulfate sodium, and analyzed the incidence of colitis-associated colon cancer. Mice conditionally lacking afadin in the intestines showed significantly increased the incidence of colon cancer. These results indicate the uppressive role of afadin in developing colitis-associated colon cancer in mice.
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