| Project/Area Number |
15K09983
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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 |
Radiation science
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| Research Institution | Hokkaido University |
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Principal Investigator |
Yasui Hironobu 北海道大学, アイソトープ総合センター, 准教授 (10570228)
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| Co-Investigator(Kenkyū-buntansha) |
山盛 徹 北海道大学, 獣医学研究院, 准教授 (00512675)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 固形腫瘍 / 放射線 / Idタンパク質 / 細胞老化 / p53 / Inhibitor of DNA binding / 腫瘍 / 転写調節因子 / p21 |
|---|
| Outline of Final Research Achievements |
Recently, inhibitor of differentiation/DNA binding 1 (Id1) has been reported to play an important role in cellular processes such as proliferation and metastasis in cancer cells. However, the role of Id1 in the radioresistance of cancer cells remains unclear. In this study, knockdown of Id1 by its specific siRNA enhanced radiosensitivity of A549 cells expressing wild-type p53, but had little effect on HeLa or HT29 cells with aberrant p53 status. The population of senescent cells remarkably increased after X-irradiation in A549 cells, and this increase was enhanced by knockdown of Id1. X-ray-induced expression of p21, a key regulator for cellular senescence, was significantly higher in Id1-knockdowned cells compared with control cells. These results indicate that Id1 contributes to the radioresistance of cancer cells via downregulation of radiation-induced senescence, suggesting that Id1 is a potent target to increase the effectiveness of cancer radiotherapy in some types of cancer.
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