槲皮素通过STAT3信号通路抑制肺癌A549细胞迁移和侵袭

Effects of quercetin on suppressing migration and invasion of A549 cells via the STAT3 signaling pathway

目的观察槲皮素通过抑制信号转导和转录激活因子3(STAT3)信号通路对肺腺癌A549细胞增殖、迁移和侵袭能力的影响。方法体外培养A549细胞,以不同浓度(0、7.5、15、30、60、120μmol/L)槲皮素处理24、48和72 h,采用CCK-8检测槲皮素对A549细胞增殖的抑制作用,计算半数抑制浓度(IC_(50))。A549细胞随机分为4组:分别以0(空白对照组)、15和30μmol/L槲皮素和3μg/ml顺铂(阳性对照组)处理24 h。采用细胞黏附实验、划痕修复实验、Transwell小室体外侵袭实验观察A549细胞黏附、迁移、侵袭能力,Western印迹法检测STAT3、磷酸化信号转导和转录激活因子3(p-STAT3)蛋白表达的变化。结果槲皮素剂量依赖性地抑制A549细胞增殖。与空白对照组相比,槲皮素显著抑制A549细胞黏附率、迁移率、侵袭细胞数(P<0.05或P<0.01);与空白对照组相比,槲皮素显著降低A549细胞STAT3和p-STAT3蛋白表达(P<0.05或P<0.01)。结论槲皮素具有明显的抑制A549细胞增殖、迁移和侵袭能力的作用,其机制可能与抑制STAT3信号通路有关。

Objective To investigate the effect of quercetin on suppressing the proliferation,migration and invasion of A549 cells via the signal transducer and activator of transcription 3（STAT3）signaling pathway. Methods The A549 cells were cultured in vitro and treated with quercetin at various concentrations（0,7.5,15,30,60 and 120μmol/L）for 24 h,48 h and 72 h. The proliferation of A549 and the 50%inhibitory concentration（IC50）were measured by the cell counting kit-8（CCK-8）. The A549 cells treated for 24 h were randomly divided into 4 groups：the blank control,15 and 30 μmol/L quercetin,and 3 μg/ml cisplatin（the positive control） groups. The effect of quercetin on adhesion rate was detected by the cell adhesion assay;the cell migration ability was evaluated by the wound healing assay;the cell invasion ability was evaluated by the Transwell chamber assay;the expression of STAT3 and phosphory？lated-STAT3（p-STAT3）proteins were detected by Western blot assay. Results Quercetin inhibited A549 cell growth dose-depend？ently. Compared with the blank control group,quercetin could significantly inhibit the adhesion rate,migration ability and invasion of A549 cells（P〈0.05 or P〈0.01）;compared with the blank control group,quercetin significantly inhibited STAT3 and p-STAT3 ex？pression level（P〈0.05 or P〈0.01）. Conclusion Quercetin could inhibit the proliferation,migration and invasion of A549 cells, and the mechanism is libely related to the STAT3 signal pathway.