| Project/Area Number |
24591365
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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 |
Endocrinology
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| Research Institution | The University of Tokushima |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
IWATA Takeo 徳島大学, 大学院ヘルスバイオサイエンス研究部, 助教 (10350399)
MIZUSAWA Noriko 徳島大学, 大学院ヘルスバイオサイエンス研究部, 助教 (80254746)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 下垂体 / 腫瘍化 / microRNA / ACTH産生腺腫 / 下垂体腺腫 / miRNA / 腫瘍 |
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| Outline of Final Research Achievements |
Transfection of miR-551b, which were underexpressed in human ACTH-producing pituitary adenomas, was found to suppress cell growth of AtT-20 cells, a cell line of mouse ACTH-producing tumors.
We found several human ACTH-producing adenomas in which high expression of ERBB4 mRNA, one of target candidate genes of miR-551b, were observed. We confirmed that ERBB4 mRNA was a target of miR-551b by co-tranfection of miR-551b and a reporter plasmid including luciferase-ERBB4 3'-untranslated region in HEK293 cells. Positive correlation between low expression of miR-551b and methylation status of CpG islands in the possible promoter of miR-551b gene was not found.
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