Background: Glioblastoma multiforme (GBM) is a highly aggressive brain tumor with poor prognosis, highlighting the need for novel therapeutic approaches. Vimentin plays a critical role in cancer cell motility, with elevated expression observed in various cancers. This study aimed to evaluate the effects of L-sarcolysine (L-S) on the migration and adhesion of U-87 cells, with a particular focus on vimentin. Methods: VIM expression and its prognostic significance were assessed in GBM tissue samples and cells. Molecular docking was performed to elucidate the binding interactions between L-S and vimentin, with emphasis on phosphorylation sites. Experimentally, the effects of L-S on viability, proliferation, apoptosis, migration, adhesion, and gene expression were evaluated in U-87 cells. Results and Conclusion: Upregulation of VIM was detected in both GBM tissues and U-87 cells. Molecular docking demonstrated that L-S interacts with vimentin at key residues involved in filament stabilization, including Ser39. In vitro assays showed that L-S significantly inhibited U-87 cell migration (p < 0.01), enhanced cell adhesion to the ECM (p < 0.01), and modulated VIM expression (p < 0.05). Collectively, these findings underscore the potential of L-S as an effective anti-migratory agent and highlight innovative therapeutic strategies targeting intermediate filaments.

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