DJ-1 regulating anticancer resistance through suppressing p53
| Project/Area Number |
25830071
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Tumor biology
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| Research Institution | Hokkaido University |
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Principal Investigator |
KATO Izumi 北海道大学, 薬学研究科(研究院), 助教 (40634994)
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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 |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | DJ-1 / p53 / がん / 酸化ストレス / 癌 / 分子間相互作用 |
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| Outline of Final Research Achievements |
The effect of cancer cell death increases depending on the ROS (Reactive Oxygen Species) in pancreatic cancer cells after anti-cancer therapy. DJ-1 binds to p53 and suppresses the transactivation activity of p53 depending on the p53-DNA binding affinity. The survival rate of pancreatic cancer patients who express high level of DJ-1 reduces by half. Therefore, cell death suppression by oxidative stress was predicted to work the malignant alteration of pancreatic cancer. We revealed the interaction between anticancer drug resistance and DJ-1. Furthermore, the relationship between anticancer drug resistance and DJ-1 or p53 was estimated by using the pancreatic cancer cells with different anticancer drug resistance.
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Report
(4 results)
Research Products
(7 results)
