Stimulation of cultured colon 26 cells with TNF-α promotes lung metastasis through the extracellular signal-regulated kinase pathway
Stimulation of cultured colon 26 cells with TNF-α promotes lung metastasis through the extracellular signal-regulated kinase pathway
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DOI：
10.1016/j.canlet.2004.12.027
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发表时间：
2005-12-08
期刊：
影响因子：
9.7
通讯作者：
Saiki, I
中科院分区：
文献类型：
--
作者：
Choo, MK;Sakurai, H;Saiki, I
我们研究了肿瘤坏死因子-α对肿瘤细胞转移的影响。用肿瘤坏死因子-α处理培养的结肠26细胞可增强转移特性，包括产生基质金属蛋白酶-9、黏附、迁移和侵袭。在体外用肿瘤坏死因子-a处理的细胞在体内显示出显著的转移到肺和肝脏的潜力。MEK1/2的抑制剂U0126可在不影响细胞增殖的前提下，抑制肿瘤坏死因子-α诱导的细胞外信号调节激酶1/2(ERK1/2)的激活及其体外转移特性。此外，U0126体外预处理可完全阻断肿瘤坏死因子-α处理细胞增加的肺转移。这些结果表明，肿瘤坏死因子-α通过ERK途径激活癌细胞足以增强结肠26细胞的转移潜能。(C)2005爱思唯尔爱尔兰有限公司。保留所有权利。
We investigated the influence of TNF-alpha on the metastasis of cancer cells. Treatment of cultured colon 26 cells with TNF-a enhanced metastatic properties including production of MMP-9, adhesion, migration and invasion. Cells treated with TNF-a in vitro showed marked potential to metastasize to the lung and liver in vivo. U0126, an inhibitor of MEK1/2, inhibited the TNF-alpha-induced activation of extracellular signal-regulated kinase 1/2 (ERK1/2) and the metastatic properties in vitro without affecting cell proliferation. In addition, pretreatment with U0126 in vitro completely abrogated the increased lung metastasis of TNF-alpha-treated cells. These results indicate that TNF-a-induced activation of cancer cells through the ERK pathway is sufficient for the enhanced metastatic potential of colon 26 cells. (c) 2005 Elsevier Ireland Ltd. All rights reserved.