| Project/Area Number |
25640092
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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 therapeutics
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| Research Institution | Iwate Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
SAKYO Tomoko 岩手医科大学, 薬学部・細胞病態生物学講座, 助教 (00405755)
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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 |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 腫瘍生物学 / がん化学療法 / 分子標的治療薬 / 糖輸送タンパク質 / 糖代謝 / 膜たんぱく質 / GSK3阻害剤 / がん分子標的薬 / がん / 分子標的薬 / 化学ライブラリー / シグナル伝達 / エキソソーム |
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| Outline of Final Research Achievements |
Increased glucose uptake is fundamental to many solid tumors and well associated with increases in glycolysis and the over-expression of glucose transporters (GLUT) at the plasma membrane. Tumor-suppressed HeLa hybrid cells express GLUT1 alone, whereas the tumorigenic HeLa cell hybrids express GLUT1 and GLUT3, which were shown to be differential distribution within the plasma membranes. In previous studies, we identified GSK-3 inhibitors that selectively kill GLUT3-expressing tumorigenic HeLa cell hybrids by using a cell-based screening of compounds in chemical libraries (Oncogenesis 2012). In this study, we found inhibition of cell growth and GLUT3-expression by GSK-3 inhibitor was also evident in human colon cancers. In addition, GSK-3 inhibitor showed a partial inhibitory effect on the in vivo tumor growth of CGL4 cells. These results suggest a potential use of GSK-3 inhibitors to selectively kill cancer cells that modulate GLUT3-dependent glucose metabolism.
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