A study for molecular mechanism of the Cdk-Pin1 axis in cancer stem cell
| Project/Area Number |
25830087
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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 | Yokohama City University |
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Principal Investigator |
NISHI Mayuko 横浜市立大学, 医学(系)研究科(研究院), 特任助教 (90635343)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 癌幹細胞 / リン酸化 / 癌抑制遺伝子 / 細胞老化 |
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| Outline of Final Research Achievements |
We recently established an induced cancer stem cell (CSC)-like model. We utilized the cell model for drug screening to inhibit the Cdk-Pin1 axis in CSCs. Withaferin A (WA) was identified as a compound inhibiting Cdk activity by inducing p21. WA inhibited not only the stemness and self-renewal properties of CSCs but also their ability of migration and invasion. WA decreased both the tumor initiation and the tumor-forming ability of CSCs in an immunosuppressed mouse model. We further attempted to identify functional Cdk substarates by a protomic approach using Pin1 as a molecular probe. We indentified several target proteins for further analysis.
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Report
(3 results)
Research Products
(5 results)
