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

Abstract

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. Key words: 1-Phosphatidylinositol 3-kinase; Protein kinase C; Propofol; Carcinoma, non-small-cell lung; Cell movement