Kiss Z, Tomono M, Anderson W B
Hormel Institute, University of Minnesota, Austin 55912.
Biochem J. 1994 Sep 15;302 ( Pt 3)(Pt 3):649-54. doi: 10.1042/bj3020649.
The phospholipase D (PLD)-mediated synthesis of phosphatidylethanol (PtdEtOH) and the hydrolysis of phosphatidylethanolamine (PtdEtn) and phosphatidylcholine (PtdCho) were examined in drug-sensitive and multidrug-resistant lines of MCF-7 human breast carcinoma cells. In drug-sensitive (MCF-7/WT) cells, the protein kinase C (PKC) activator phorbol 12-myristate 13-acetate (PMA) failed to enhance either the synthesis of PtdEtOH or the hydrolysis of either phospholipid. In the drug-resistant (MCF-7/MDR) cells, 100 nM PMA greatly enhanced both the synthesis of PtdEtOH (approximately 21-fold) and the hydrolysis of PtdEtn (approximately 29-fold), but had no effect on the hydrolysis of PtdCho. The PLD activators sphingosine and H2O2 were found to elicit only a slight (1.28-1.4-fold) stimulatory effect on PtdCho hydrolysis in both the MCF-7/WT and MCF-7/MDR cell types, and had only a small effect on PtdEtn hydrolysis in the MCF-7/WT cells as well. However, these agents significantly (approximately 2.6-3.5-fold) stimulated PtdEtn hydrolysis in the MCF-7/MDR cells. These data indicate that MCF-7/MDR cells contain a PtdEtn-specific PLD activity which can be selectively stimulated by PMA, sphingosine and H2O2.
在MCF-7人乳腺癌细胞的药物敏感和多药耐药系中，研究了磷脂酶D（PLD）介导的磷脂酰乙醇（PtdEtOH）合成以及磷脂酰乙醇胺（PtdEtn）和磷脂酰胆碱（PtdCho）的水解。在药物敏感（MCF-7/WT）细胞中，蛋白激酶C（PKC）激活剂佛波醇12-肉豆蔻酸酯13-乙酸酯（PMA）未能增强PtdEtOH的合成或任何一种磷脂的水解。在耐药（MCF-7/MDR）细胞中，100 nM PMA极大地增强了PtdEtOH的合成（约21倍）和PtdEtn的水解（约29倍），但对PtdCho的水解没有影响。发现PLD激活剂鞘氨醇和H2O2对MCF-7/WT和MCF-7/MDR两种细胞类型的PtdCho水解仅产生轻微的（1.28 - 1.4倍）刺激作用，对MCF-7/WT细胞中的PtdEtn水解也只有很小的影响。然而，这些试剂显著（约2.6 - 3.5倍）刺激了MCF-7/MDR细胞中的PtdEtn水解。这些数据表明，MCF-7/MDR细胞含有一种PtdEtn特异性PLD活性，其可被PMA、鞘氨醇和H2O2选择性刺激。
