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J. Biochem, 1988, Vol. 104, No. 1 53-56
© 1988 Japanese Biochemical Society

research-article

Inhibition of DNA Synthesis by Protein Kinase C-Activating Phorbol Esters in NIH/3T3 Cells1

Takeshi Yamamoto, Terutaka Tsuda, Yasuo Hamamori, Noriyuki Nishimura and Yoshimi Takai2

Department of Biochemistry, Kobe University School of Medicine Chuo-ku, Kobe, Hyogo 650

2 To whom correspondence should be addressed

Fibroblast growth factor (FGF) plus insulin induced DNA synthesis in and proliferation of NIH/3T3 cells. The protein kinase C-activating phorbol ester, 12-o-tetradecanoylphorbol 13-acetate (TPA), inhibited both the DNA synthesis and cell proliferation induced by FGF plus insulin. The concentration of TPA required for50% inhibition of the DNA synthesis was about 5 nM. Phorbol-12,13-dibutyrate, another protein kinase C-activating phorbol ester, also inhibited the DNA synthesis but 4{alpha}-phorbol-12,13-didecanoate, known to be inactive for this enzyme, was ineffective. DNA synthesis started at about 12 h after the addition of FGF plus insulin. The inhibitory action of TPA on the DNA synthesis was observed when it was added within 12 h after the addition of FGF plus insulin. These results suggest that phorbol esters exhibit an antiproliferative action through protein kinase C activation in NIH/3T3 cells, and that this action of phorbol esters is due to inhibition of the progression from the late G1 to the S phase of the cell cycle.

1This investigation was supported in part by research grants from the Scientific Research Fund of the Ministry of Education, Science and Culture of Japan (1987), the Investigation Committee on Abnormal ities in Hormone Receptor Mechanisms, the Ministry of Health and Welfare of Japan (1987), the Yamanouchi Foundation for Research on Metabolic Disorders (1987), and the Research Program on Cell Calcium Signals in the Cardiovascular System (1987)


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