Search and function elucidation of lncRNAs that regulate epithelial-mesenchymal transition
| Project/Area Number |
18K06057
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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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| Review Section |
Basic Section 43010:Molecular biology-related
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| Research Institution | Kanazawa University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
鈴木 健之 金沢大学, がん進展制御研究所, 教授 (30262075)
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2020: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2019: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2018: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 上皮間葉転換 / EMT / 長鎖非コードRNA / lncRNA / ポリコーム抑制複合体 / PRC2 / 上皮間葉転換（EMT) / 長鎖非コードRNA (lncRNA) / エピジェネティック調節因子 / 遺伝子発現制御 |
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| Outline of Final Research Achievements |
We have focused on epithelial-mesenchymal transition (EMT) as a mechanism of cancer progression and reported that polycomb repressive complex (PRC2), which is one of epigenetic regulators, induces EMT by repressing the expression of epithelial genes. Furthermore, MEG3 long noncoding RNA contributes to epigenetic regulation of EMT by guiding PRC2 to its target gene loci. In this study, we proposed that RIAN (MEG8) long noncoding RNA, which shares the DLK1-DIO3 locus with MEG3, is involved in EMT in a different manner from MEG3. These results contribute to understanding of long noncoding RNA involved in cancer progression.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究は、EMTの制御に関与するlncRNAの探索・同定とその機能解析から、EMTのエピジェネティック調節を司る新しい機能性分子としてのlncRNAの役割を明らかにする。これは、腫瘍の悪性進展を導くlncRNAの機能を解明するものであり、この成果を基盤として、lncRNAの新しいがん治療標的としての可能性を開拓できる。
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Report
(4 results)
Research Products
(11 results)
