| Project/Area Number |
26462184
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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 |
Neurosurgery
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| Research Institution | Kochi University |
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Principal Investigator |
UEBA Tetsuya 高知大学, 教育研究部医療学系臨床医学部門, 教授 (00314203)
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| Co-Investigator(Kenkyū-buntansha) |
八幡 俊男 高知大学, 教育研究部医療学系臨床医学部門, 助教 (40380323)
東 洋一郎 高知大学, 教育研究部医療学系基礎医学部門, 助教 (80380062)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 膠芽腫 / エピジェネティクス / DNAメチル化 / 脳腫瘍 / メチル化DNA結合タンパク / エピゲネティクス |
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| Outline of Final Research Achievements |
MBD1 (Methyl-CpG-binding domain protein 1) binds to methylated CpG and is involved in transcriptional repression and then plays an essential role in transmitting epigenetic information. In glioblastoma (GBM), aberrant splicing of MBD1 has been observed as a post transcriptional mechanism. Shorter isoform of MBD1 is little expressed in normal cells, but is predominantly expressed in GBM. In this study, we analyzed the splicing regulation and function of the tumor-specific isoform. A reporter system was developed for detecting the aberrant splicing of MBD1. Knockdown of the tumor-specific isoform induced growth inhibition in GBM cells. These results suggest that the aberrant splicing of MBD1 contributes to oncogenesis and oncogenic phenotypes.
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