| Project/Area Number |
22700878
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Tumor biology
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
KAWAUCHI Junya 東京医科歯科大学, 難治疾患研究所, 助教 (20544498)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2012: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2010: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | がん抑制遺伝子 / p53 / PolII / FCP1 / CCFDN / 転写 / 脱リン酸化 / 細胞増殖 |
|---|
| Research Abstract |
p53 is one of the tumor-suppressor genes which frequently have mutations in human cancer. FCP1 e-phosphorylates Pol II in order to re-cycle for the next round transcription at or after transcription termination. In this grant period, we found the connection between FCP1 and p53, detailed as below.1. FCP1 knocking-down (siFCP1) HeLa cell showed significant growth defect along withp53 accumulation and p21 expression. Additionally, FCP1 was associated with p53 under5-FU treatment in HeLa cell, indicating that there is the link between tumor suppressor p53 and Pol II phosphatase FCP1. 2. This p21 activation required BRCT domain, but does not required RAP74 binding domain. 3. Under doxorubicin treatment, siFCP1 MCF7 cell showed marked decrease in p21 expression. We could not detect the novel p53-related substrate of FCP1, however, these results suggested that FCP1 is involved in the p53 regulation pathway.
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