Takada K, Amino N, Tetsumoto T, Miyai K
Department of Laboratory Medicine, Osaka University Medical School, Japan.
FEBS Lett. 1988 Jul 4;234(1):13-6. doi: 10.1016/0014-5793(88)81292-4.
In quiescent rat thyroid (FRTL-5) cells, phorbol-12-myristate-13-acetate (PMA) inhibited DNA synthesis induced by a combination of insulin and thyrotropin (TSH) or dibutyryl cyclic AMP (Bt2cAMP). This inhibitory effect of PMA was observed even when PMA was added after addition of these growth factors, and was maximal when PMA was added 2-4 h after the growth factors (late in the G1-phase of the cell cycle). On the other hand, PMA alone induced DNA synthesis and also enhanced that induced by Bt2cAMP or insulin in these quiescent cells. 1-Oleoyl-2-acetylglycerol mimicked these effects of PMA, but 4 alpha-phorbol-12,13-didecanoate had no effect. These data demonstrate that in FRTL-5 cells protein kinase C has a stimulatory effect on the G0 to G1 transition and an inhibitory effect on the G1 to S transition in the cell cycle.
在静止的大鼠甲状腺（FRTL-5）细胞中，佛波醇-12-肉豆蔻酸酯-13-乙酸酯（PMA）抑制胰岛素和促甲状腺激素（TSH）或二丁酰环磷腺苷（Bt2cAMP）联合诱导的DNA合成。即使在添加这些生长因子后再添加PMA，也能观察到PMA的这种抑制作用，当在生长因子添加后2-4小时（细胞周期G1期晚期）添加PMA时，抑制作用最大。另一方面，单独的PMA可诱导DNA合成，并且还增强了这些静止细胞中Bt2cAMP或胰岛素诱导的DNA合成。1-油酰基-2-乙酰甘油模拟了PMA的这些作用，但4α-佛波醇-12,13-二癸酸酯没有作用。这些数据表明，在FRTL-5细胞中，蛋白激酶C对细胞周期中从G0到G1的转变具有刺激作用，而对从G1到S的转变具有抑制作用。
