RFT gene expression in malignant transformation of gliomas
| Project/Area Number |
12671355
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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 |
Cerebral neurosurgery
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
TAKAHASHI Jun (2002) Kyoto Univ, Graduate School of Medicine, Lecture, 医学研究科, 講師 (80252435)
上羽 哲也 (2000-2001) 京都大学, 医学研究科, 助手 (00314203)
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| Co-Investigator(Kenkyū-buntansha) |
高橋 潤 京都大学, 医学研究科, 講師 (80252435)
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| Project Period (FY) |
2000 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2002: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2001: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2000: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | glioma / RFT / FGF-2 / グリオーマ / transcription / tumor suppressor gene / glioma |
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| Research Abstract |
The regulator of fibroblast growth factor (FGF)-2 transcription (RFT) has been, reported to be a transcriptional repressor of FGF-2 and induce glioma cell death by its overexpression. Here we report that RFT regulated cell cycle as well as apoptosis by a novel mechanism. RFT expressed in some glioma cell lines, U 13 8MG and T98G, but neither in U25iMG and U87MG Over expressed RFT induced apoptosis in U87MG and U138MG with functioning-type p53 but neither in U251Mg nor T98G with non-functioning-type p53. Administration of FGF-2 failed to prevent RFT induced apoptosis. Overexpression of RFT caused GI-S arrest and upregulated buts the phosphorylation of p53 at Ser-15 and the expression level of p2lwafl. Furthermore, RNAi knockdown of p53 abolished RFT induced apoptosis in U87MG. Taken together, our results support that RFT regulates Gl-S transition and apoptosis via p53/p2lwafl pathway.
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Report
(4 results)
Research Products
(9 results)
