Kiss Z, Tomono M
Hormel Institute, University of Minnesota, Austin 55912.
FEBS Lett. 1995 Jan 30;358(3):243-6. doi: 10.1016/0014-5793(94)01434-3.
We have previously reported that in C3H/10T1/2 fibroblasts the environmental carcinogen 7,12-dimethyl-benz[a]anthracene (DMBA) stimulated phosphorylation of ethanolamine (Etn). Here we show that in these fibroblasts DMBA also stimulates phosphorylation of choline (Cho). Wortmannin (50-200 nM), an established inhibitor of phosphatidylinositol-3-kinase (PI3K), significantly inhibited DMBA-induced phosphorylation of both Etn and Cho. Wortmannin also inhibited the effect of insulin, a major activator of PI3K, on DNA synthesis. However, insulin had no effect on the phosphorylation of Etn and Cho. These data suggest that a carcinogen-induced kinase phosphorylates both Etn and Cho, and that the inhibitory effect of wortmannin on Etn/Cho kinase activity may be unrelated to its inhibitory effect on PI3K activity.
我们之前报道过，在C3H/10T1/2成纤维细胞中，环境致癌物7,12-二甲基苯并[a]蒽（DMBA）可刺激乙醇胺（Etn）的磷酸化。在此我们表明，在这些成纤维细胞中，DMBA还可刺激胆碱（Cho）的磷酸化。渥曼青霉素（50 - 200 nM）是一种已确定的磷脂酰肌醇-3-激酶（PI3K）抑制剂，可显著抑制DMBA诱导的Etn和Cho的磷酸化。渥曼青霉素还可抑制胰岛素（PI3K的主要激活剂）对DNA合成的作用。然而，胰岛素对Etn和Cho的磷酸化没有影响。这些数据表明，致癌物诱导的激酶可使Etn和Cho都发生磷酸化，并且渥曼青霉素对Etn/Cho激酶活性的抑制作用可能与其对PI3K活性的抑制作用无关。
