| Project/Area Number |
25430108
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Tumor biology
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| Research Institution | Kansai Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
HIROTA Kiichi 関西医科大学, 医学部, 准教授 (00283606)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 腎癌 / デオキシグルコース / ABT-263 / AKT / beta-cyclodextrin / アポトーシス / コレシテロール / 膵臓がん / シグナル伝達 / インスリン / 抗がん剤 / コレステロール / 受容体型チロシンキナーゼ / Mcl１ / Bak / Caveolin / アポプトーシス / デオコシグルコース / エンドサイトーシス |
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| Outline of Final Research Achievements |
2-DG is taken-up by highly glycolytic cells such as muscle cells under heavy exercise, brain cells and cancer cells. Since ABT cannot cross the blood-brain barrier, only cells exposed to both agents under normal treatment conditions are cancer cells, and these are only cells that are induced into apoptosis. However, 2DG-ABT combination was less effective in renal cancer cells. We discovered that highly activated AKT was the reason for the resistance in these cancer cells. When we inhibited AKT by beta-cyclodextrin, 2DG-ABT became more effective.
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