2015 Fiscal Year Final Research Report
The molecular mechanism of 2deoxyglucose-ABT-263 induced apoptosis
| 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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| Keywords | 腎癌 / デオキシグルコース / ABT-263 / AKT / beta-cyclodextrin / アポトーシス |
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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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| Free Research Field |
腫瘍学
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