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首页> 美国卫生研究院文献>Neoplasia (New York N.Y.) >Exposure of Human Breast Cancer Cells to the Anti-inflammatory Agent Indomethacin Alters Choline Phospholipid Metabolites and Nm23 Expression
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Exposure of Human Breast Cancer Cells to the Anti-inflammatory Agent Indomethacin Alters Choline Phospholipid Metabolites and Nm23 Expression

机译：人类乳腺癌细胞暴露于消炎药消炎痛改变胆碱磷脂代谢产物和Nm23表达。

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We previously observed that changes in choline phospholipids of two malignant human mammary epithelial cells (HMECs) following treatment with a high dose of the cyclooxygenase (COX) inhibitor, indomethacin, mimicked changes following transfection with a metastasis suppressor gene, nm23. The similarity between response to indomethacin and nm23 transfection led us to 1) expand our 1H NMR spectroscopy study of indomethacin treatment by determining the response at two doses for two nonmalignant and three malignant HMECs, 2) investigate COX-1 and COX-2 levels in HMECs and their relationship with choline phosholipid metabolites, and 3) determine changes in Nm23 expression following treatment with indomethacin. All HMECs exhibited a significant change in choline phospholipids following treatment with 300 µM indomethacin. At the lower dose of 50 µM, only nonmalignant HMECs and the estrogen-dependent malignant cell line, MCF-7, responded. COX-1 levels were significantly higher in malignant HMECs than in nonmalignant HMECs. A significant increase in Nm23 expression following 300 µM indomethacin was detected in MCF-12A and MCF-7 cells but not in MDA-MB-231 and MDAMB-435 cells. These results suggest that COX-1 expression and its inhibition play a role in the choline phospholipid metabolism of HMECs, and the effect of indomethacin on HMECs may be mediated, in part, through upregulation of nm23.
机译：我们以前观察到，用高剂量的环氧合酶（COX）抑制剂吲哚美辛治疗后，两个恶性人乳腺上皮细胞（HMEC）的胆碱磷脂变化模仿了转移抑制基因nm23转染后的变化。对消炎痛和nm23转染的反应之间的相似性导致我们：1）通过确定两种剂量对两种非恶性和三种恶性HMEC的反应，扩大了消炎痛治疗的 1 H NMR光谱研究，2）研究了COX HMEC中的-1和COX-2水平及其与胆碱磷脂代谢产物的关系，以及3）确定消炎痛治疗后Nm23表达的变化。用300 µM消炎痛处理后，所有HMEC的胆碱磷脂均发生显着变化。在50 µM的较低剂量下，只有非恶性HMEC和依赖雌激素的恶性细胞系MCF-7才有反应。恶性HMEC中的COX-1水平显着高于非恶性HMEC。在MCF-12A和MCF-7细胞中检测到300μM消炎痛后Nm23表达显着增加，而在MDA-MB-231和MDAMB-435细胞中未检测到。这些结果表明，COX-1的表达及其抑制作用在HMEC的胆碱磷脂代谢中起作用，吲哚美辛对HMEC的作用可能部分地通过nm23的上调来介导。

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