| Project/Area Number |
10671669
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Pediatric surgery
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| Research Institution | Osaka University |
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Principal Investigator |
WASA Masafumi Osaka University, Graduate School of Medicine, Assistant Profess, 医学系研究科, 助手 (10240467)
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| Co-Investigator(Kenkyū-buntansha) |
OKADA Akira Osaka University, Graduate School of Medicine, Professor, 医学系研究科, 教授 (40028569)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥2,600,000 (Direct Cost: ¥2,600,000)
Fiscal Year 1999: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1998: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | neuroblastoma / IGF-I / Glutamine / amino acid transport / 小児悪性腫瘍 |
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| Research Abstract |
It is still unknown how insulin-like growth factor-I (IGF-I) regulates cancer cell growth in the condition of the limited availability of key nutrients, such as glutamine. We investigated the effects of IGF-I on cell growth and amino acid transport in aglutamine-deprived human neuroblastoma cell line, SK-N-SH.Cell growth was measured, and ^3H-amino acid transport was assayed after treatment with or without IGF-I (50 ng/ml) in 2 mM (control) and 100 μM glutamine concentrations. Cell growth rates were dependent on glutamine concentrations. IGF-I stimulated cell growth in both 2 mM and 100 μM glutamine. IGF-I stimulated glutamine transport in 100 μM glutamine with the mechanism of increasing carrier Vmax, but had no effect in 2 mM glutaunine There were significant increases in ^3H-thymidine and ^3H-leucine incorporation in IGF-I treated cells in both 2 mM and 100 μM glutamine. In the presence of the monoclonal antibody against the type I IGF receptor (IGF-IR), cell proliferation was significantly attenuated and glutamine transport was decreased. These data suggest that IGF-I/IGF-IR interaction stimulates cell growth by increasing amino acid transport in the condition of low glutamine levels in a human neuroblastoma cell line. This mechanism may allow to maintain cell growth even in nutrients-deprived tumor tissues.
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