Figure 3

IL-17 promotes HCC invasion via AKT-dependent IL-6/STAT3 activation. SMMC7721 cells were exposed to AKT-targeted or STAT3-targeted siRNA, and then cultured with IL-17 (50 ng/ml) and/or IL-6 (100 ng/ml) for 24 h. (A) As assessed by ELISA, the expression of IL-6, IL-8, MMP2 and VEGF showed no significant change after IL-17 stimulation in siRNA-AKT-SMMC7721 cells, while expression of IL-8, MMP2 and VEGF were significantly increased after addition of IL-17 plus IL-6. (B) AKT-siRNA significantly downregulated JAK2/STAT3 phosphorylation induced by IL-17. (C) IL-6 also recovered IL-17-stimulated JAK2/STAT3 phosphorylation in siRNA-AKT-SMMC7721 cells. (D) As shown by Matrigel invasion assay, STAT3-siRNA significantly reversed tumor invasion by IL-17 stimulation. IL-6 mAb (10 ng/ml for 36 h) completely reversed IL-17-induced HCC invasion, while IL-6 (100 ng/ml for 36 h) completely recovered IL-17-stimulated invasion of siRNA-AKT-SMMC7721 cells. Three separate experiments were performed in each study. Data are expressed as mean ± SD; Student's t test; # p > 0.05; *p < 0.05, **p < 0.01, and ***p < 0.001.