2018 Fiscal Year Final Research Report
Novel strategies for cancer stem cells
Project/Area Number |
16K10454
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
General surgery
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Research Institution | Nagoya University |
Principal Investigator |
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Co-Investigator(Kenkyū-buntansha) |
梛野 正人 名古屋大学, 医学系研究科, 教授 (20237564)
横山 幸浩 名古屋大学, 医学系研究科, 寄附講座教授 (80378091)
國料 俊男 名古屋大学, 医学部附属病院, 講師 (60378023)
山口 淳平 名古屋大学, 医学部附属病院, 助教 (00566987)
|
Project Period (FY) |
2016-04-01 – 2019-03-31
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Keywords | 融合遺伝子 / 癌幹細胞 |
Outline of Final Research Achievements |
Proliferation was activated in c-Met-positive cholangiocarcinoma cells compared with that in c-Met-negative cholangiocarcinoma cells. Cell viability was suppressed in c-Met-positive and CD49f-positive cholangiocarcinoma cells. Cell growth was more highly activated in CD133-positive colorectal cancer cells than in CD133-negative colorectal cancer cells. Next-generation sequencing revealed 938 candidate fusion genes in cancer cells. LOC646214, which is a p21 protein (Cdc42/Rac)-activated kinase 2 pseudogene, formed fusions with many genes. In addition, long intergenic/intervening noncoding RNA (LINC) formed fusions with many genes. Because these fusion genes do not synthesize proteins, antibody medicines were not effective against these genes. From this viewpoint, these fusion genes were thought to be the best targets for nucleic acid medicines.
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Free Research Field |
消化器外科学
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Academic Significance and Societal Importance of the Research Achievements |
本研究により、次世代シークエンサーによる融合遺伝子の探索により、p21 protein (Cdc42/Rac)-activated kinase 2 pseudogeneであるLOC646214が多くの遺伝子と融合遺伝子を形成していることを明らかにした。新たな融合遺伝子の候補の同定、核酸医薬による新規癌治療の可能性を明らかにしており、本研究成果の学術的、社会的意義は大きい。
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