PI3K/Akt信号通路在异丙酚抑制人非小细胞肺癌H1975细胞迁移和侵袭力中的作用

Role of PI3K/Akt signaling pathway in propofol-induced inhibition of migration and invasion ability of human non-small cell lung cancer H1975 cells

目的评价磷脂酰肌醇-3-激酶/丝氨酸-苏氨酸激酶(PI3K/Akt)信号通路在异丙酚抑制人非小细胞肺癌H1975细胞迁移和侵袭力中的作用。方法采用随机数字表法将H1975细胞分为4组(n=36):对照组(C组)、20 μg/ml异丙酚组(P组)、0.5 ng/ml PI3K/Akt信号通路激动剂类胰岛素一号增长因子IGF-1组(IGF-1组)和20 μg/ml异丙酚+ 0.5 ng/ml IGF-1组(P+ IGF-1组)。用划痕实验和Transwell侵袭实验分别检测细胞的迁移和侵袭力,并用Western blot法检测细胞Akt、磷酸化Akt(p-Akt)及基质金属蛋白酶-9(MMP-9)的表达。结果与C组比较,P组细胞迁移和侵袭力减弱,p-Akt和MMP-9表达下调(P<0.05);IGF-1组H1975细胞迁移和侵袭力增强,p-Akt和MMP-9表达上调(P<0.05);与P组比较,P+IGF-1组细胞迁移和侵袭力增强,p-Akt和MMP-9表达上调(P<0.05);与IGF-1组比较,P+IGF-1组细胞迁移和侵袭力减弱,p-Akt和MMP-9表达下调(P<0.05)。结论异丙酚抑制人非小细胞肺癌H1975细胞迁移和侵袭力的机制与阻断PI3K/Akt信号通路有关。

Objective To evaluate the role of phosphatidylinositol 3-kinase/serine-threonine kinase (PI3K/Akt) signaling pathway in propofol-induced inhibition of migration and invasion ability of human non-small cell lung cancer H1975 cells. Methods H1975 cells were divided into 4 groups(n=36 each)using a random number table method: control group (group C), 20 μg/ml propofol group (group P), 0.5 ng/ml PI3K/Akt signaling pathway activator insulin-like growth factor 1 (IGF-1) group (group IGF-1), and 20 μg/ml propofol plus 0.5 ng/ml IGF-1 group (group P+ IGF-1). The migration and invasion ability of H1975 cells was determined by wound healing assay and Transwell invasion assay, respectively.The expression of phosphorylated Akt (p-Akt) and matrix metalloproteinase-9 (MMP-9) was assessed by Western blot. Results Compared with group C, and the ability of migration and invasion was significantly reduced, and the expression of p-Akt and MMP-9 was down-regulated in group P, and the ability of migration and invasion was significantly enhanced, and the expression of p-Akt and MMP-9 was up-regulated in group IGF-1 (P<0.05). Compared with group P, the ability of migration and invasion was significantly enhanced, and the expression of p-Akt and MMP-9 was up-regulated in group P+ IGF-1 (P<0.05). Compared with group IGF-1, the ability of migration and invasion was significantly reduced, and the expression of p-Akt and MMP-9 was down-regulated in group P+ IGF-1 (P<0.05). Conclusion The mechanism by which propofol inhibits migration and invasion ability of human non-small cell lung cancer H1975 cells is related to blocking PI3K/Akt signaling pathway.