Overexpression of RFT induces G1-S arrest and apoptosis via p53/p21Waf1 pathway in glioma cell

被引：7
|
作者：
Kano, H
Arakawa, Y
Takahashi, JA
Nozaki, K
Kawabata, Y
Takatsuka, K
Kageyama, R
Ueba, T [1 ]
Hashimoto, N
机构：
[1] Kyoto Univ, Grad Sch Med, Dept Neurosurg, Sakyo Ku, Kyoto 6068315, Japan
[2] Kyoto Univ, Grad Sch Med, Dept Pharmacol, Sakyo Ku, Kyoto 6068315, Japan
[3] Kishiwada City Hosp, Dept Neurosurg, Osaka 5968501, Japan
[4] Kyoto Univ, Inst Virus Res, Kyoto 6068507, Japan
来源：
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2004年 / 317卷 / 03期
关键词：
RFT; FGF-2; p53; p21(Waf1); cell cycle; apoptosis;
D O I：
10.1016/j.bbrc.2004.03.120
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
The regulator of fibroblast growth factor 2 (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 regulates cell cycle as well as apoptosis by a novel mechanism. RFT expressed in some glioma cell lines, U138MG and T98G, but neither in U87MG nor U251MG. Overexpressed 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 G1-S arrest and upregulated both the phosphorylation of p53 at Ser-15 and the expression level of p21(Waf1).. Furthermore, RNAi knockdown of p53 abolished RFT-induced apoptosis in U87MG. Taken together, our results support that RFT regulates G1-S transition and apoptosis via p53/p21(Waf1) pathway. (C) 2004 Elsevier Inc. All rights reserved.
引用
收藏
页码：902 / 908
页数：7
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