Induction of instability of p34cdc2 expression by treatment with cisplatin (CDDP) in mouse teratocarcinoma F9 cells

被引:7
作者
Doi, T
Morita, T
Wakabayashi, N
Sumi, T
Iwai, SA
Amekawa, S
Sakuda, M
Nishimune, Y
机构
[1] Osaka Univ, Microbial Dis Res Inst, Suita, Osaka 565, Japan
[2] Osaka Univ, Fac Dent, Dept Oral & Maxillofacial Surg 2, Osaka, Japan
[3] Osaka City Univ, Sch Med, Dept Mol Genet, Osaka 545, Japan
[4] Univ Tsukuba, Ctr Tsukuba Adv Res Alliance, Tsukuba, Ibaraki 305, Japan
[5] Univ Tsukuba, Inst Basic Med Sci, Tsukuba, Ibaraki 305, Japan
关键词
cis-diamminedichloroplatinum (II); p34(cdc2); teratocarcinoma F9 cell;
D O I
10.1016/S0304-3835(01)00579-1
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
p34(cdc2) is a protein kinase that plays an important role in the control of the cell cycle and regulation of activity of the tumor suppressor gene. Previously, we demonstrated that cisplatin (CDDP) induced growth suppression resulting in differentiation of teratocarcinoma F9 cells. In the present study, we investigated the mechanism of cell cycle retardation by CDDP in F9 cells, focusing on P34(cdc2). After the induction of differentiation with CDDP, F9 cells were arrested at the late S + G2/M. After treatment with CDDP, the level of the expression of cdc2 mRNA did not change. However, the half-life of p34(cdc2) was greatly reduced, thus, the level of p34(cdc2) protein was decreased. These findings suggest that the cell cycle arrest by CDDP is due partly to the induced instability of p34(cdc2) in F9 cells. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.
引用
收藏
页码:75 / 80
页数:6
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