| Project/Area Number |
26640083
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Tumor biology
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| Research Institution | Kumamoto University |
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Principal Investigator |
Nambu Akiko 熊本大学, その他の研究科, 特別研究員 (40572087)
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| Co-Investigator(Renkei-kenkyūsha) |
Araki Norie 熊本大学, 大学院生命科学研究部, 准教授 (80253722)
Narimatsu Hisashi 独立行政法人産業技術総合研究所, 糖鎖医工学研究センター, 教授 (40129581)
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| Research Collaborator |
Nagai Minako 熊本大学, 大学院生命科学研究部, 研究技術員
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | がん幹細胞 / 脳腫瘍 / グライコプロテオミクス / 糖鎖 / プロテオグリカン / 分化 / 微小環境 / 分化ニッチ / 糖鎖タンパク質 / プロテオーム |
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| Outline of Final Research Achievements |
In this study, to clarify the molecular mechanisms of GSC differentiation, we established GSC clones having the potential to differentiate into glioblastoma, and subjected to lectin microarray, quantitative real-time PCR (qPCR) array, and integrated proteomics for glyco-protein expression profiling. These analyses revealed that the expression of proteoglycan, including chondroitin sulfate proteoglycan such as CSPG4, and chondroitin sulfate synthetic enzymes/transferase, such as Xylosyltransferase 1/2 (XYLT1/2), were significantly downregulated during serum-induced GSC differentiation. Treatments of chondroitin sulfate degradation enzyme (chABC) significantly induced GSC differentiation, but the chondroitin and CSPG si RNA inhibited the GSC differentiation. These results indicate that CSPG is a key regulator of GSC maintenance/differentiation, and is a potential clinical target against malignant glioma.
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