Myristoylated alanine‑rich C‑kinase substrate (MARCKS) serves an important role in various pathological processes in several malignancies. However, little is known about the specific role and molecular mechanism of MARCKS in glioblastoma (GBM). In the present study, it was found that the expression of MARCKS was significantly upregulated in GBM, and was associated with a poor clinical outcome in patients with GBM. Knockdown of MARCKS suppressed the migration and invasion of GBM cells in vitro. Western blotting showed that the knockdown of MARCKS reduced the expression of phosphorylated phosphoinositide 3‑kinase and protein kinase B, as well as zinc finger protein SNAI1 expression, thereby modulating the expression of its downstream epithelial‑mesenchymal transition (EMT)‑associated factors, including E‑cadherin, vimentin, N‑cadherin and β‑catenin in GBM cells. These results indicate that MARCKS functioned in the migration and invasion of GBM, and therefore may provide a potential therapeutic target in GBM therapy.