| Project/Area Number |
26870576
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Pathological medical chemistry
Tumor biology
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| Research Institution | Keio University |
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Principal Investigator |
Tabata Sho 慶應義塾大学, 政策・メディア研究科(藤沢), 特任助教 (30708342)
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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: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | thymidine catabolism / thymidine phosphorylase / 解糖系 / thymidine |
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| Outline of Final Research Achievements |
Thymidine phosphorylase (TP), a rate-limiting enzyme in thymidine catabolism, plays a pivotal role in tumor progression; however, the mechanisms underlying this role are not fully understood. Here, we found that TP-mediated thymidine catabolism could supply the carbon source in the glycolytic pathway and thus contribute to cell survival under conditions of nutrient deprivation. In TP-expressing cells, thymidine was converted to metabolites including glucose 6-phosphate, lactate and 5-phosphoribosyl 1α-diphosphate via the glycolytic pathway both in vitro and in vivo. These thymidine-derived metabolites were required for the survival of cells in low glucose conditions. Furthermore, energy metabolism activated by thymidine catabolism was observed in human gastric cancer. These findings demonstrate that thymidine can serve as a novel energy source in human cancer cells.
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