Overexpression of RFT induces G1-S arrest and apoptosis via p53/p21 super(Waf1) pathway in glioma cell

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 gliom...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2004-05, Vol.317 (3), p.902-908
Main Authors: Kano, H, Arakawa, Y, Takahashi, JA, Nozaki, K, Kawabata, Y, Takatsuka, K, Kageyama, R, Ueba, T, Hashimoto, N
Format: Article
Language:English
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Summary: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 super(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 super(Waf1) pathway.
ISSN:0006-291X
DOI:10.1016/j.bbrc.2004.03.120