Downregulation of ERK signaling impairs U2OS osteosarcoma cell migration in collagen matrix by suppressing MMP9 production.
Downregulation of ERK signaling impairs U2OS osteosarcoma cell migration in collagen matrix by suppressing MMP9 production.
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DOI：
10.3892/ol.2013.1655
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发表时间：
2014-01
期刊：
影响因子：
2.9
通讯作者：
Kim DK
中科院分区：
文献类型：
--
作者：
Poudel B;Kim DK;Ki HH;Kwon YB;Lee YM;Kim DK
本研究探讨了细胞外信号调节激酶（ERK）激活在胶原基质中人U2OS骨肉瘤（OS）细胞迁移表型中的作用。ERK激酶特异性抑制剂PD98059可抑制ERK的激活。此外，在胶原包被的培养皿中，在有或没有PD98059处理的情况下，细胞的粘附和增殖没有观察到显著差异。然后在未包被和胶原包被的培养皿中检查U2OS细胞的迁移能力，结果显示胶原I增强了U2OS细胞的迁移，其效果被用PD98059处理的细胞显著阻断。此外，基质金属蛋白酶9（MMP 9），而不是MMP 2的基因和蛋白质表达增强，被观察到参与增强迁移表型的U20 S细胞在胶原包被的板。用ERK抑制剂处理胶原包被的培养皿中的细胞可部分消除这种作用。总的来说，这些数据表明ERK信号传导通过增强MMP 9的产生对于U2OS细胞通过主要由胶原蛋白组成的细胞外基质（ECM）的迁移是重要的。这些结果可能有助于MMP9在转移性OS中的产生的调节。
The present study investigated the role of extracellular signal-regulated kinase (ERK) activation in the migratory phenotype of human U2OS osteosarcoma (OS) cells in a collagen matrix. The activation of ERK was inhibited by PD98059, a specific inhibitor of ERK kinase. Additionally, no significant differences were observed in the adhesion and proliferation of the cells with or without PD98059 treatment in collagen-coated dishes. The migratory capacity of the U2OS cells was then examined in non-coated and collagen-coated dishes, and the results depicted that collagen I enhanced the migration of the U2OS cells, the effect of which was significantly blocked by the treatment of the cells with PD98059. Furthermore, enhanced gene and protein expression of matrix metalloproteinase 9 (MMP9), but not MMP2, was observed to be involved in the enhanced migratory phenotype of the U20S cells in the collagen-coated plates. This effect was partially abolished by the treatment of the cells in the collagen-coated dishes with ERK inhibitor. Collectively, the data demonstrate that ERK signaling is important for the migration of U2OS cells through the extracellular matrix (ECM), which is comprised mostly of collagen, by enhancing MMP9 production. These results may contribute to the regulation of MMP9 production in metastatic OS.
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