目的：研究白介素8（IL-8）对食管鳞癌细胞株KYSE170 迁移能力的影响，并初步探讨其作用机制。方法：体外合成针对IL-8 的siRNA，采用脂质体法转染KYSE170 细胞，利用Real-time PCR和Wsetern blotting 及ELISA 法检测沉默效率，镜下观察细胞形态学改变，划痕实验检测细胞迁移能力，CCK-8 实验检测细胞增殖能力的变化。Wsetern blotting 检测IL-8 受体及JAK2-STAT3 信号通路相关蛋白的表达。结果：与阴性对照组比较，靶向沉默IL-8 处理后的KYSE170 细胞，其IL-8 基因和蛋白表达水平均明显降低（P<0.01），IL-8 分泌量显著减少（P<0.01）；IL-8 基因沉默后，KYSE170 细胞迁移能力明显减弱（P<0.01），而细胞增殖能力无明显变化。IL-8 受体2 即CXCR2、转移相关蛋白WASF3 的表达水平明显降低（P<0.05），而IL-8 受体1 即CXCR1的表达水平没有明显变化；JAK2-STAT3 信号通路关键蛋白p-JAK2 和p-STAT3 表达明显降低（均P<0.01）。结论：下调IL-8 的表达可以抑制食管癌细胞株KYSE170的迁移能力，其机制可能通过介导CXCR2 及其下游JAK2-STAT3信号通路活性的改变相关。

Objective: To investigate the effect of interleukin-8 (IL-8) on esophageal cancer cell line KYSE170, and to preliminarily explore its mechanism. Methods: siRNA targeting IL-8 was in vitro synthesized and transfected into KYSE170 cells by lipofectamine 2000. The efficiency of silencing was determined by Real-time PCR, Western blotting and ELISA. Morphological changes of KYSE170 cells were observed microscopically. Scratch assay was performed to observe the cell migration ability. CCK-8 assay was used to detect the cell proliferation ability. Western blotting was used to detect the expressions of IL-8 receptor and JAK2-STAT3 signaling pathway related proteins. Results: Compared with the negative control group, the mRNA and protein expressions of IL-8 in KYSE170 cells were all significantly decreased after IL-8 silencing (P<0.01), and IL-8 secretion was significantly reduced (P<0.01). After IL-8 gene silencing,the migration capacity of KYSE170 cells was significantly weakened (P<0.01), while no significant changes in cell proliferation was detected. The expression of IL-8 receptor 2 (CXCR2) and transfer-related protein WASF3 were significantly decreased (P<0.05), while the expression of IL-8 receptor 1 (CXCR1) was not significantly changed; the expressions of p-JAK2 and p-STAT3 protein in JAK2-STAT3 signaling pathway were significantly decreased (all P<0.01). Conclusion: Knock-down of IL-8 inhibits the migration of esophageal cancer KYSE170 cells, and the mechanism may be related with the alteration of CXCR2 and its downstream JAK2-STAT3 signaling pathway.

河北省科技计划项目资助（No.162777249）