图 3.

ANXA2的降低通过AKT/cofilin通路抑制肺腺癌细胞中CCL18诱导的F-肌动蛋白聚合。A：在不同时长的10 ng/mL CCL18的刺激下Scr/A549以及和SiANXA2#2/A549细胞中相对F-actin含量；B：在CCL18刺激下，分析Scr/A549、SiANXA2#2/A549中p-AKT（Ser473）、p-AKT（Thr308）的表达水平，实验中使用AKT和β-actin用作阴性对照；C：分析在CCL18的刺激下，Scr/A549、SiANXA2#2/A549中cofilin、LIMK的表达水平，实验中使用cofilin、LIMK和β-actin用作阴性对照。

The reduction of ANXA2 inhibits CCL18-induced F-actin polymerization in lung adenocarcinoma cells through the AKT/cofilin pathway. A: Relative F-actin content in Scr/A549 and SiANXA2#2/A549 cells stimulated by 10 ng/mL CCL18 at different times; B: Under the stimulation of CCL18, the expression levels of p-AKT (Ser473) and p-AKT (Thr308) in Scr/A549 and SiANXA2#2/A549 were analyzed by Western blot analysis. AKT and β-actin were used as negative contrast in the experiment; C: Analyze the expression levels of cofilin and LIMK in Scr/A549, SiANXA2#2/A549 under the stimulation of CCL18 by Western blot analysis. In the experiment, cofilin, LIMK and β-actin were used as negative controls.