| Project/Area Number |
18K07977
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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 53010:Gastroenterology-related
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| Research Institution | Sapporo Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
鈴木 拓 札幌医科大学, 医学部, 教授 (20381254)
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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 |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2020: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2019: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2018: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | 消化器がん / エピジェネティクス / noncoding RNA / long noncoding RNA / 胃癌 / 大腸癌 / lncRNA |
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| Outline of Final Research Achievements |
In this study, we analyzed the expression of lncRNA in gastrointestinal tumors by using publicly available TCGA database and compared that in normal tissues or tumors. We tested several methods to select the prospective lncRNA genes and analyzed the function of selected lncRNAs. Among them, we assessed the function of lncX gene. Depletion of lncX by using specific siRNA reduced cell viability and induced apoptosis in several cancer cells. To investigate the effects on gene expression profiles by knockdown of lncX, we performed gene expression microarray analysis. Accordingly, we found that a number of genes regulating cell cycle were significantly downregulated. We confirmed the reduction of AURKA, cyclin B1, and survivin. Then, we performed luciferase reporter assay by using promoter of AURKA gene. We assessed the effects of lncX with WT CED or Mut CED reporter. Consequently, results of reporter assay suggest that lncX is involve to the activation of cell cycle genes.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究では消化管がんの増殖を抑制するノンコーディングRNA分子を発見しています。この分子を抑制することで腫瘍細胞の細胞死が誘導される事や、細胞分裂に関連する遺伝子群を制御していることが明らかとなりました。詳細なメカニズムについてはこれからさらに解析する必用がありますが、この分子は正常では発現が低いために、この分子を標的とする治療はがんに特異的なものになる可能性があると考えられます。
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