| Project/Area Number |
16K08636
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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 |
Pathological medical chemistry
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| Research Institution | National Center for Geriatrics and Gerontology |
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Principal Investigator |
YAMAKOSHI Kimi 国立研究開発法人国立長寿医療研究センター, 老化機構研究部, 室長 (50423398)
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| Research Collaborator |
KAMEYAMA Akihiko
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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 |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2018: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | がん / 糖鎖 / ムチン / 癌 / 遺伝子 / 細胞・組織 / 老化 |
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| Outline of Final Research Achievements |
Bmi-1, a core component of the polycomb repressive complex 1 (PRC1), is dysregulated in various types of cancer, and its upregulation strongly correlates with invasive phenotype and poor prognosis in patients with certain types of carcinoma. In addition, changes in glycosylation of cell-surface glycoconjugates are also known to be associated with tumor malignancy. However, the relationship between Bmi-1 and altered glycosylation as to invasiveness has not been elucidated. In this study, we found that the expression of the GCNT3 gene, which encodes mucin-type core 2 1, 6-N-acetylglucosaminyltransferase enzyme was suppressed by Bmi-1. In addition, we demonstrated that GCNT3 has a function to suppress the proliferation and invasive behavior of abnormal cells through core 2 O-glycans.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究の遂行により、がんとコア2糖鎖の関係の詳細を分子メカニズムから解明した。本研究の成果は、がんと糖鎖の関係について新たな知見を提供し、がん化のメカニズムについての理解を促進すると考えられる。また、本成果は、がんの予防や治療に応用できる可能性があり、人類の福祉に大きく貢献できることが期待される。
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