Author/Authors :
Doi، نويسنده , , Toshihide and Morita، نويسنده , , Takashi and Wakabayashi، نويسنده , , Nobunao and Sumi، نويسنده , , Tetsuro and Iwai، نويسنده , , Souichi A. and Amekawa، نويسنده , , Shigeki and Sakuda، نويسنده , , Masayoshi and Nishimune، نويسنده , , Yoshitake، نويسنده ,
Abstract :
p34cdc2 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 p34cdc2. 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 p34cdc2 was greatly reduced, thus, the level of p34cdc2 protein was decreased. These findings suggest that the cell cycle arrest by CDDP is due partly to the induced instability of p34cdc2 in F9 cells.
