目的：探讨IL-17A对结肠癌细胞株SW480侵袭、迁移的作用及其机制。方法: 体外培养结肠癌SW480细胞，分为实验组(IL-17A 50 ng/ml)及对照组(空白组)。通过细胞划痕实验观察细胞的迁移能力，Transwell侵袭实验检测细胞的侵袭能力， Western blotting检测细胞MMP-2/9蛋白及 PI3k/AKT/NF-κB通路相关蛋白的表达水平。结果: 经50 ng/ml的IL-17A处理后，（1）SW480细胞的迁移距离及穿膜细胞数目均明显增加\[(2.49±0.18） vs （1.54±021) mm及(262.00±2460）vs （92.00±31.16)个，均P<0.05\]；（2）SW480细胞MMP-2/9蛋白水平明显上调\[（0.41±005） vs （0.23±0.03）及（0.76±009） vs （0.25±0.04），均P<0.05\]；（3）SW480细胞AKT磷酸化水平表达增加\[（0.72±0.1） vs（0.28±0.04），P<0.05\]，P65和P50蛋白表达水平明显升高\[(0.78±0.10) vs (0.35±0.04)和(0.85±0.15) vs (044±006), 均P<0.05\], 而c-Rel、ReLB和P52蛋白表达无明显变化（P>0.05）。结论: IL-17A诱导结肠癌SW480细胞迁移和侵袭, 其机制可能与激活PI3K/AKT/NF-κB转导通路、调节MMP-2/9蛋白表达有关。

Objective:To explore the effect and mechanism of IL-17A on invasion and migration of colon cancer SW480 cells.Methods: Colon cancer SW480 cells were in vitro cultured and divided into experimental group (IL-17A 50 ng/ml) and control group (blank group). The migration ability was observed by cell scratch assay, the invasion feature of SW480 cells was detected by Transwell assay, and the expressions of MMP-2/9 protein and PI3k/AKT/NF-κ B pathway related proteins were tested by Western blotting. Results: After the treatment with IL-17A(50 ng/ml), (1) the migration distance and trans-membrane number of SW480 cells significantly increased (\[2.49±018\] mm vs \[1.54±0.21\] mm; \[262.00±24.60\] vs \[92.00±31.16\]; all P<0.05); (2) the expression of MMP-2/9 protein in SW480 cells was obviously up-regulated (\[0.41±0.05\] vs \[0.23±0.03\]; \[0.76±0.09\] vs \[0.25±0.04\], all P<0.05); (3) AKT-phosphorylation level in SW480 cells was significantly increased (\[0.72±0.1\] vs \[028±0.04\], P<0.05), and the protein expressions of P65 and P50 were significantly increased (\[0.78±0.10\] vs \[0.35±0.04\]; \[0.85±0.15\] vs \[0.44±0.06\], all P<0.05); however, the protein expressions of c-Rel, ReLB, and P52 showed no significant difference (P>0.05). Conclusion: IL-17A induced the migration and invasion of colon cancer SW480 cells, and increased tumor cell viability; the mechanism may be related to the activation of PI3K/AKT/NF-κB pathway and up-regulation of MMP-2/9 protein expression.

辽宁省教育厅科学技术一般项目（No.L2014333）