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Mefenamic acid-induced apoptosis in human liver cancer cell-lines through caspase-3 pathway

机译:甲芬那酸通过caspase-3途径诱导人肝癌细胞凋亡

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摘要

Non-steroidal anti-inflammatory drugs (NSAIDs) have anti-proliferative effects and induce apoptosis in colon and other cancers. In the present study, we report that mefenamic acid (MEF), a member of NSAIDs, has an inhibitory effect on a proliferation of liver cancer cells. We used Chang and Huh-7 cells as human liver cancer cells. MEF-treated Huh-7 and Chang cells displayed apoptotic morphological changes and the portion of cells in sub G1 was increased 3-fold and 6-fold, respectively, at a 200 muM concentration. We also show an MEF-enhanced binding of annexin V to cells and an increased activity of caspase-3 to cleave PARP-1 and caspase itself. The inhibitor of caspase-3 blocked PARP-1 cleavage activity and protected against MEF-induced apoptotic cell death. These results indicate that MEF induces apoptosis in human liver cancer cells. (C) 2004 Elsevier Inc. All rights reserved.
机译:非甾体类抗炎药(NSAIDs)具有抗增殖作用,并诱导结肠癌和其他癌症的细胞凋亡。在本研究中,我们报告说,NSAIDs的成员甲芬那酸(MEF)对肝癌细胞的增殖具有抑制作用。我们将Chang和Huh-7细胞用作人类肝癌细胞。 MEF处理的Huh-7和Chang细胞显示出凋亡的形态变化,并且在200μM的浓度下,sub G1中的细胞部分分别增加了3倍和6倍。我们还显示出膜联蛋白V与细胞的MEF增强结合以及caspase-3裂解PARP-1和caspase本身的活性增加。 caspase-3抑制剂可阻断PARP-1的切割活性,并防止MEF诱导的凋亡细胞死亡。这些结果表明MEF诱导人肝癌细胞的凋亡。 (C)2004 Elsevier Inc.保留所有权利。

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