| Project/Area Number |
25860247
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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
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| Research Institution | Showa University |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | がん / 足場依存的生存 / 代謝 / DICD / アノイキス |
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| Outline of Final Research Achievements |
In this study, we investigated the relationship between detachment-induced cell death (DICD) and changes in glucose metabolism for a better understanding of resistance to DICD acquired by metastatic cancer cells. First, we observed the accumulation of fructose-6-phosphate (F6P) in normal human mammary epithelial cells during DICD. Because F6P is a metabolic intermediate in both glycolysis and the hexamine pathways and detachment scarcely suppressed glycolysis, it was assumed that the hexamine pathway was suppressed in response to detachment, which resulted in DICD. To examine whether inhibition of the hexamine pathway is sufficient to induce cell death, we used the inhibitor of the rate-limiting enzyme, azaserine, in the hexamine pathway. Treatment with azaserine remarkably evoked cell death even under adherent condition. Thus, it was suggested that DICD may be mediated by repression of the hexamine pathway.
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