| Project/Area Number |
23590162
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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 |
Environmental pharmacy
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| Research Institution | National Center of Neurology and Psychiatry (2013)
Research Institute for Clinical Oncology, Saitama Cancer Center (2011-2012) |
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Principal Investigator |
SHIIZAKI Kazuhiro 独立行政法人国立がん研究センター, 研究所, 研究員 (20391112)
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| Co-Investigator(Renkei-kenkyūsha) |
IKUTA Togo 埼玉県立がんセンター, 臨床腫瘍研究所, 主任研究員 (00262072)
KAWAJIRI Kaname 埼玉県立がんセンター, 臨床腫瘍研究所, 客員研究員 (50142112)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | AhR / β-catenin / 大腸がん / リガンド / CUL4B / 盲腸 / βカテニン / 盲腸内容物 |
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| Research Abstract |
It was reported that beta-catenin, which plays a critical role in the development of colorectal cancer, was degraded by aryl hydrocarbon receptor (AhR) in a ligand dependent manner. Confirmatory experiments of the relationship between AhR and beta-catenin were carried out in various colon cancer cell lines, but the beta-catenin degradation by AhR ligand treatment could not be observed. Furthermore, reporter assay and two-hybrid assay failed to identify the interaction between beta-catenin, CUL4B, and AhR.
On the other hand, the spontaneous tumorigenesis in AhR-deficient mouse cecum was reconfirmed. It was speculated that some kind of ligand activated AhR and prevented tumorigenesis in cecum. The AhR ligand-like activities were detected in cecal contents of wild-type mice by using improved yeast reporter assay system. By the HPLC analysis, AhR ligand-like activity was found in several fractions.
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