Background: Propofol has been identified to perform anti-tumor functions in glioma. However, the molecular mechanisms underlying propofol-induced prevention on migration and invasion of glioma cells remain unclear.
Methods: Cell proliferation, invasion and migration were measured by 3-(4,5)-dimethylthiahiazo(−z-y1)-3,5-di-phenytetrazoliumromide assay and transwell assay, respectively. The expression of microRNA (miR)-206 and Rho-associated coiled coil-containing protein kinase 1 (ROCK1) was detected by quantitative real-time polymerase chain reaction. Western blot was used to measure the activation of the PI3K/AKT pathway. The interaction between miR-206 and ROCK1 was analyzed using the dual-luciferase reporter assay, RNA immunoprecipitation assay, and pull-down assay.
Results: Propofol treatment inhibited the migration, invasion, and PI3K/AKT pathway activation in glioma cells. MiR-206 was decreased in glioma tissues and cells, while propofol exposure induced the upregulation of miR-206 in glioma cells. Besides that, we also found overexpressed miR-206 enhanced propofol-mediated inhibition on the migration, invasion, and PI3K/AKT pathway activation of glioma cells. Subsequently, ROCK1 was confirmed to be a target of miR-206. ROCK1 was elevated in glioma tissues and cells, but was reduced by propofol exposure in glioma cells. The rescue assay indicated that the miR-206/ROCK1 axis was involved in propofol-induced inhibition on the migration, invasion, and PI3K/AKT pathway activation in glioma cells.
Conclusion: Propofol inhibited the migration and invasion of glioma cells by blocking the PI3K/AKT pathway through the miR-206/ROCK1 axis, suggesting an effective clinical implication for the anesthetic to prevent the metastasis of glioma.
Keywords: propofol, miR-206, ROCK1, glioma, PI3K/AKT pathway