Reverse Glycomics Clarification of Resistance Mechanism for Leukemia Cell and Development of Diagnosis Method for Antitumor Drug Resistance
| Project/Area Number |
26505008
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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 |
オミクス計測科学
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| Research Institution | Hiroshima University |
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Principal Investigator |
Nakano Miyako 広島大学, 先端物質科学研究科, 准教授 (40397724)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 糖鎖分析 / 白血病 / 薬剤耐性 / グライコミクス / 診断法 |
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| Outline of Final Research Achievements |
The main treatment of leukemia is chemotherapy using antitumor drugs, but the acquisition of drug resistance often makes treatment continuation impossible. The mechanism of acquired drug resistance must be elucidated. We focused on glycan structures on cell-membrane proteins. A leukemia cell line (CEM) was selected for acquired drug resistance against an antitumor drug (dEpoB), and glycan structures on the cell-membrane proteins was analyzed. The resistant cell line (CEM/dEpoB) showed a significant decrease of 2-6 sialylated N-glycans. The reduction was cause of 2-6 sialyltransferase 1 (ST6GAL1) gene. To ascertain the cause-and-effect relationship between reduction of 2-6 sialylated N-glycans and acquired drug resistance, we knock-downed and transfected the ST6GAL1 gene. The CEM with the knock-down ST6GAL1 gene showed acquired drug resistance. This result suggests that reduction in the 2-6 sialylation could be the cause of dEpoB-resistance acquisition.
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Report
(4 results)
Research Products
(8 results)
