Research for imainmotherany by iron-chelation against hepatocellular carcinoma
| Project/Area Number |
18590515
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Applied pharmacology
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| Research Institution | Dokkyo Medical University |
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Principal Investigator |
KUBOTA Keiichi Dokkyo Medical University, Medicine, Professor (70260388)
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| Co-Investigator(Kenkyū-buntansha) |
SAWADA Tokihiko Dokkyo Medical University, Medicine, Associate professor (20266761)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥2,630,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥330,000)
Fiscal Year 2007: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2006: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | hepatocellular carcinoma / colon cancer / iron-chelation / interferonY / apoptosis / DFO / 鉄イオン |
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| Research Abstract |
Interferon y (IFNy) exerts its effect by biding to the specific receptor. IFNy receptor comprise of R1 and R2 subunits. In normal cells and cancer cells, R1 is constitutively expressed, but R2 is usually downregulated. Downregulation of R2 results in the resistance of cancer cells to anti-neoplastic effect of IFNy. It is necessary to increase the expression of R2 in cancer cells, in order to increase the susceptibility to IFNy. Because it has been shown that iron-chelation increase the expression of R2 in T cell lymphoma, we tested the effect of the iron-chelation in hepatocellular carcinoma (in year of 2006) and colon cancer (in year 2007). In both cancer cells, iron-chelation effectively increased the expression of R2, and resulted in increased susceptibility of IFNy, including growth inhibition and apoptosis-induction. It is suggested that iron-chelation. Plus IFNy is promising new method to treat hepatocellular carcinoma and colon cancer.
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Report
(3 results)
Research Products
(11 results)
