Objective To investigate the effect of vecuronium bromide (VB) on the proliferation and metastasis of human non-small cell lung cancer A549 cells and its possible mechanism.
Methods Drug toxicity testing was used to screen appropriate dosage of VB. Cell counting kit-8 (CCK-8) was used to detect cell proliferation. Hoechst staining was used to detect cell apoptosis. Transwell and wound healing were used to detect cell metastasis; Western blot was used to detect expressions of phosphatidylinositol-3-kinase/protein kinase B (PI3K/AKT) pathway-related proteins.
Results Compared to those of the control cells, the A549 cells treated with VB showed significantly decreased proliferation, increased apoptosis rate, increased number of invading cells, decreased wound closure rate, significantly decreased expressions of PI3K, phosphorylated PI3K (p-PI3K) and hypoxia-inducible factor-1 alpha (HIF-1α), and increased ratios of PI3K/AKT and phosphorylated mammalian target of rapamycin (p-mTOR)/mTOR; while, the A549 cells treated with 740Y-P (a PI3K agonist) exhibited increased proliferation, apoptosis rate, the number of invading cells, wound closure rate, expressions of PI3K, p-PI3K and HIF-1α, and ratios of PI3K/AKT p-mTOR/mTOR. Whereas, in comparison with the A549 cells treated only with 740Y-P, the A549 cells treated with both VB and 740Y-P demonstrated decreased proliferation, the number of invading cells, wound closure rate, expressions of PI3K, p-PI3K and HIF-1α, and ratios of PI3K/AKT p-mTOR/mTOR but increased apoptosis rate.
Conclusion Vecuronium bromide can obviously inhibit the proliferation and metastasis of A549 cells possibly by inhibiting the PI3K/AKT pathway.
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