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首页> 外文期刊>Oncogene >Interleukin-18 is a critical factor for vascular endothelial growth factor-enhanced migration in human gastric cancer cell lines
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Interleukin-18 is a critical factor for vascular endothelial growth factor-enhanced migration in human gastric cancer cell lines

机译：白细胞介素18是人类胃癌细胞系中血管内皮生长因子增强迁移的关键因素

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Cell migration and angiogenesis are key steps in tumor metastasis. However, the mechanism of migration regulated by vascular endothelial growth factor (VEGF), a potent regulator of angiogenesis, is not completely understood. This study examined the relationship between VEGF and migration, along with the mechanism involved in the VEGF-regulated migration of human gastric cancer cells. The level of cell migration was increased by recombinant human (rh)VEGF-165 in the VEGF receptor-2-expressing SNU-601 cells. Interleukin (IL)-18 is associated with the malignant progression of tumors. Accordingly, this study examined the effect of IL-18 on the migration of cancer cells in order to identify the factors involved in VEGF-enhanced migration. Inhibiting IL-18 markedly reduced the level of VEGF-enhanced migration, and IL-18 increased cell migration directly through filamentous-actin polymerization and tensin downregulation. It was confirmed that rhVEGF-165 increased IL-18 production significantly. An antioxidant and an extracellular signal-regulated kinase (ERK)1/2-specific inhibitor blocked rhVEGF-165-enhanced IL-18 production. Accordingly, rhVEGF-165 increased the generation of region of interest (ROI) and activated the ERK1/2 pathway. These results suggest that rhVEGF-165 enhances IL-18 production via the generation of ROI and ERK1/2 phosphorylation, which results in the increased migration of gastric cancer cells.
机译：细胞迁移和血管生成是肿瘤转移的关键步骤。但是，尚未完全了解由血管内皮生长因子（VEGF）（一种有效的血管生成调节剂）调节的迁移机制。这项研究检查了VEGF与迁移之间的关系，以及涉及VEGF调控的人胃癌细胞迁移的机制。重组人（rh）VEGF-165在表达VEGF受体2的SNU-601细胞中增加了细胞迁移的水平。白介素（IL）-18与肿瘤的恶性进展有关。因此，本研究检查了IL-18对癌细胞迁移的影响，以鉴定参与VEGF增强迁移的因素。抑制IL-18可显着降低VEGF增强的迁移水平，而IL-18可直接通过丝状肌动蛋白聚合和张力蛋白下调直接增加细胞迁移。证实rhVEGF-165显着增加了IL-18的产生。抗氧化剂和细胞外信号调节激酶（ERK）1/2特异性抑制剂可阻止rhVEGF-165增强的IL-18产生。因此，rhVEGF-165增加了感兴趣区域（ROI）的生成并激活了ERK1 / 2途径。这些结果表明，rhVEGF-165通过ROI和ERK1 / 2磷酸化的产生增强IL-18的产生，这导致胃癌细胞迁移的增加。

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