Mechanism of tumour heterogeneity mediated by mRNA processing
| Project/Area Number |
16K09314
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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 |
Gastroenterology
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| Research Institution | The University of Tokushima |
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Principal Investigator |
NISHIDA Kensei 徳島大学, 大学院医歯薬学研究部(医学域), 准教授 (10624033)
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| Research Collaborator |
TANAKA Hiroki
KUWANO Yuki
ROKUTAN Kazuhito
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | ヘテロジェナイティ / 大腸がん / 上皮間葉移行 / RNAプロセシング / DNAメチル化 / マイクロRNA / microRNA / migration / DNA methylation / mRNAプロセシング |
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| Outline of Final Research Achievements |
We purified a subpopulation of cells from the colon cancer cell line HCT116, which had high migration capacity. Using this subpopulation, we investigated novel factors involved in migrating capacity. We had following findings: (1) identifiation of 35 up-regulated genes in mRNA expression, whose promoter region were hypermethylated and (2) identification of a microRNA cluster, which is upregulated in gene expression, in acquiring increased migratory capabilities in colon cancer cells.
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| Academic Significance and Societal Importance of the Research Achievements |
がんの遊走能獲得は、浸潤・転移などのがんの悪性形質獲得における重要な形質となる。本研究で同定に成功した、（１）遊走能獲得過程でDNAメチル化を介して発現が制御される遺伝子、ならびに（２）発現が上昇するmicroRNAクラスターは、大腸がんの進展・悪性化を制御する分子生物学的メカニズムの解明ならびに、治療ターゲットの開発に役立つ可能性が示唆された。
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Report
(4 results)
Research Products
(5 results)
