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首页> 外文期刊>Journal of Cellular Physiology >Stromal cell-derived factor-1/CXC receptor 4 and β1 integrin interaction regulates urokinase-type plasminogen activator expression in human colorectal cancer cells
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Stromal cell-derived factor-1/CXC receptor 4 and β1 integrin interaction regulates urokinase-type plasminogen activator expression in human colorectal cancer cells

机译：基质细胞衍生因子- 1科学家受体4β1整合素相互作用调节urokinase-type纤溶酶原激活物表达在人类结直肠癌细胞

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摘要

The stromal cell-derived factor-1 (SDF-1)/CXC receptor 4 (CXCR4) axis has been shown to play a role in colorectal cancer progression. In addition, the protease urokinase-type plasminogen activator (uPA) is an important factor in tumor cell invasion and metastasis. However, the mechanism by which SDF-1 mediates uPA expression in human colorectal cancer cells remains unknown. We investigated the molecular mechanism governing the interaction between SDF-1 stimulation and uPA expression in three human colon cancer cell lines (DLD-1, SW48, and COLO 205). We found that SDF-1 stimulation led to an increase in the expression and secretion of uPA in these cells. Experiments involving specific inhibitors and small interfering RNA demonstrated that the activation of p38 mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kinase (PI3K)/Akt pathways are critical for SDF-1-induced uPA expression. Analysis of transcription factor binding using ELISA and chromatin immunoprecipitation assays revealed that SDF-1 increased Sp1- and AP-1-DNA-binding activities in DLD-1 cells. Inhibition of Sp1 and AP-1 activation blocked the SDF-1-induced expression and activity of the uPA promoter. The effect of SDF-1 on DLD-1 signaling and uPA expression was mediated by the CXCR4/β1 integrin axis. In summary, our findings elucidate the mechanisms of SDF-1/CXCR4 downstream signaling and provide insights into the function of SDF-1 in colon cancer cells.
机译：基质细胞衍生因子- 1 (SDF-1) /科学家受体4 (CXCR4)轴可以发挥在大肠癌进展中的作用。而且,蛋白酶urokinase-type纤溶酶原。物活化剂(uPA)是肿瘤的一个重要因素细胞的浸润和转移。机制SDF-1介导uPA表达式在人类大肠癌细胞仍然是未知的。我们调查了分子机制管理之间的交互和uPA SDF-1刺激在三人结肠癌细胞系表达(科罗拉多州DLD-1 SW48, 205)。刺激导致增加表达式在这些细胞和分泌uPA。涉及特定抑制剂和小干扰RNA表明激活p38增殖作用的蛋白激酶(MAPK)和磷脂酰肌醇3-kinase PI3K / Akt通路SDF-1-induced uPA至关重要表达式。绑定使用ELISA和染色质免疫沉淀反应化验表明SDF-1增加了Sp1和AP-1-DNA-binding活动DLD-1细胞。激活了SDF-1-induced表达式uPA启动子和活动。SDF-1 DLD-1信号和uPA表达式趋化因子受体CXCR4 /β1整合素介导的轴。总结,我们发现机制的阐明SDF-1 / CXCR4下游信号并提供洞察SDF-1在结肠的功能癌细胞。

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