Induction of instability of p34(cdc2) expression by treatment with cisplatin (CDDP) in mouse teratocarcinoma F9 cells.

Abstract

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.

• Authors: Toshihide Doi, Takashi Morita, Nobunao Wakabayashi, Tetsuro Sumi, Souichi A Iwai, Shigeki Amekawa, Masayoshi Sakuda, Yoshitake Nishimune
• Journal: Cancer letters (Cancer Lett) Vol. 176 Issue 1 Pg. 75-80 (Feb 08 2002) ISSN: 0304-3835 [Print] Ireland
• PMID: 11790456 (Publication Type: Journal Article)

Chemical References

• Antineoplastic Agents
• RNA, Messenger
• CDC2 Protein Kinase
• Cisplatin

Topics

• Animals
• Antineoplastic Agents (pharmacology)
• Blotting, Northern
• Blotting, Western
• CDC2 Protein Kinase (biosynthesis, genetics)
• Cell Cycle
• Cisplatin (pharmacology)
• Mice
• Precipitin Tests
• RNA, Messenger (metabolism)
• Teratocarcinoma (drug therapy, metabolism)
• Time Factors
• Tumor Cells, Cultured