Tamoxifen stimulates phospholipase D activity by an estrogen receptor‐independent mechanism

FEBS Letters

Kiss, Zoltan¹ 

[1] The Hormel Institute, University of Minnesota, 801 16th Avenue NE, Austin, MN 55912, USA

关键词: Tamoxifen;    Phospholipase D;    Breast cancer;    Fibroblast;    TAM;    tamoxifen;    PKC;    protein kinase C;    PLD;    phospholipase D;    PtdEtn;    phosphatidylethanolamine;    PtdCho;    phosphatidylcholine;    PtdEtOH;    phosphatidylethanol;    PMA;    phorbol 12-myristate 13-acetate;   

DOI  :  10.1016/0014-5793(94)01200-8

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

The effects of tamoxifen (TAM), a widely used agent in the treatment of breast cancer, were examined on phospholipase D (PLD)-mediated phospholipid hydrolysis. In drug-sensitive MCF-7 human breast carcinoma cells TAM, similar to several well-established activators of PLD, had no effect on phospholipid hydrolysis. In an estrogen receptor-deficient multidrug-resistant subline of MCF-7 cells, TAM preferentially stimulated the hydrolysis of phosphatidylethanolamine; two-fold stimulation required 2.5 or 5 μM TAM in the absence or presence of serum, respectively. In NIH 3T3 fibroblasts significant (4- to 4.8-fold) stimulation of phosphatidylethanolamine and phosphatidylcholine hydrolysis in the presence of serum required 10 μM TAM. These data establish that TAM can stimulate PLD activity by an estrogen receptor-independent mechanism.

【 授权许可】

Unknown