| Project/Area Number |
10470496
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
医薬分子機能学
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| Research Institution | The University of Tokushima |
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Principal Investigator |
TERADA Hiroshi Fac. Pharm. Sci., Univ. Tokushima, Professor, 薬学部, 教授 (00035544)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAZAKI Naoshi Fac. Pharm. Sci., Univ. Tokushima, Assistant Professor, 薬学部, 助手 (20271083)
SHINOHARA Yasuo Fac. Pharm. Sci., Univ. Tokushima, Associate Professor, 薬学部, 助教授 (60226157)
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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 |
¥12,200,000 (Direct Cost: ¥12,200,000)
Fiscal Year 1999: ¥5,800,000 (Direct Cost: ¥5,800,000)
Fiscal Year 1998: ¥6,400,000 (Direct Cost: ¥6,400,000)
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| Keywords | energy metabolism / oxidative phosphorylation / mitochondria / glycolysis / antitumor drugs / type II hexokinase / type 1 glucose transporter |
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| Research Abstract |
Previously, we found that the transcript level of type II hexokinase was remarkable in malignant tumor cells. However, the molecular mechanisms which cause such drastic changes in the transcript level of type II hexokinase in tumor cells is still unknown. Thus, in this study, we tried to understand how the expression of this gene is regulated in tumor cells. We obtained following results.
1. We first explored under which condition the expression of type II hexokinase is remarkable. As a result, transcript level of type II hexokinase was remarkable when AH13O cells were grown in an abdominal cavity of rats. However, when this cell line was grown in culture dishes, the transcript level of type II hexokinase was remarkably lower than that observed with ascites cells. These results indicate that the transcript level of type II hexokinase could be changed accompanied by changes in culture conditions.
2. To understand how such remarkable change is caused, we examined possible involvement of hypoxia and serum stimulation. As a result, gene expression of type II hexokinase was remarkably elevated by serum stimulation.
Based on these results, we concluded that the metabolic pathway of sugar in tumor cells could be changed accompanied by changes in their growth conditions and that this change is mainly mediated by serum responsive factor.
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