Effect of miR449a to inhibition of tumorigenesis
| Project/Area Number |
15K08307
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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 |
Pathological medical chemistry
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| Research Institution | The University of Tokushima |
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Principal Investigator |
NISHIDA Jun 徳島大学, 大学院医歯薬学研究部(医学系), 助教 (00361981)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | マイクロRNA / がん / miR449a |
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| Outline of Final Research Achievements |
MicroRNAs and Notch signaling control cell differentiation and tumorigenesis. However, the mechanisms through which Notch mediates microRNA expression are still unclear. We found that miR449a was indirectly regulated by Notch signaling. Although miR449a-deficient mice did not show any Notch-dependent defects in immune cell development, treatment of miR-449a-deficient mice with azoxymethane and dextran sodium sulfate increased the numbers and sizes of colon tumors and intestinal epithelial cell proliferation. In patients with colon cancer, miR-449a expression was inversely correlated with histological scores and was positively correlated with the expression of MLH1. Colon tissues of miR-449a-deficient mice showed reduced Mlh1 expression compared with those of wildtype mice. Thus, these data suggested that miR-449a acted as a key regulator of colon tumorigenesis by controlling the proliferation of intestinal epithelial cells.
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Report
(4 results)
Research Products
(1 results)
