| Project/Area Number |
24790379
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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 |
Experimental pathology
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| Research Institution | University of Fukui |
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Principal Investigator |
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
|
| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | Id2 / Apc / 腸管腫瘍 / Wntシグナル / Wnt |
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| Research Abstract |
To genetically examine the physiological role of increased expression of Id2 in the intestinal tumorigenesis, we crossed the Apc delta 716 mice with the Id2-/- mice, and evaluated the polyp-number, -size, and -apoptosis in the Apc delta 716;Id2-/- (Apc;Id2) mice. Notably, lack of Id2 reduced the number of ileal polyps by ~80%, as compared with that of the control mice. On the other hand, Id2 deficiency had a little effect on the proliferation and apoptosis of the adenoma epithelium of Apc delta 716 mice. These results raise the possibilities that the elevated expression of Id2 is implicated in the process of intestinal adenoma-initiation. To further analyze the mechanisms, we next conducted DNA microarray analysis. This comprehensive analysis revealed that Id2 knockout increases expression of c-Myc antagonist gene and tumor-initiation suppressor genes. These results strongly suggest that Id2 promotes ileal adenoma initiation through suppression of those genes.
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