| Project/Area Number |
07671507
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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 | Yamanashi Medical University |
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Principal Investigator |
NAGANUMA Hirofumi Yamanashi Medical University Department of Neurosurgery Assistant Professor, 医学部, 講師 (90189142)
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| Co-Investigator(Kenkyū-buntansha) |
MAEDA Shuichiro YamanaShi Medical University First Department of Biochemistry Professor, 医学部, 教授 (10117244)
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1996: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1995: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | malignant glioma / transforming growth factor-beta / transforming growth factor-beta receptor / p27 / growth inhibition / transfomring growth factor-β / transfomring growth factor-β receptor |
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| Research Abstract |
We investigated the response of 8 malignant glioma cell lines to the growth inhibitory activity of transforming growth factor-beta (TGF-beta) in vitro and the expression of TGF-beta type I and type II receptors in malingnant glioma cells. We then investigated the effect of TGF-beta on the expression of a p27Kip1 cyclin-dependent kinase inhibitor to assess a downstream signal transmission from TGF-beta receptors. All malignant glioma cell lines were insensitive to growth inhibition by TGF-beta1 and TGF-beta2. Analysis of TGF-beta receptors by affinity labeling using 125I-TGF-beta1 showed 6 glioma lines had both TGF-beta type I and type II receptors on their cell surfaces, while 2 tumor lines had very small amount of TGF-beta type I and/or type II receptors. Northern blot analysis showed all tumor lines expressed messsenger ribonucleic acids for both TGF-beta type I and II receptors in variable levels. Flow cytometric analyzes revealed that treatment of malignant glioma cells with TGF-beta1 downregulated significantly the sxpression of p27Kip1 protein in all malignant glioma cell lines, except in one glioma line.
These data suggest that most malignant glioma cells express TGF-beta type I and type II receptors that can transmit some siganls downstream, and that loss of response to TGF-beta growth inhibition may not be due to the abnormality of TGF-beta receptors themselves.
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