Effects of Sodin 5 on the Proliferation and Migration of Human Glioblastoma Cells

Abstract

Background: Glioblastoma (GBM) is the most aggressive primary brain tumor and remains difficult to treat because of its highly invasive behavior and resistance to conventional therapies despite surgery, radiotherapy, and chemotherapy. Sodin 5, a novel type-1 ribosome-inactivating protein (RIP), inhibits protein synthesis and displays cytotoxic activity against several tumor cell types, making it a promising candidate for GBM therapy. Methods: The antitumor activity of sodin 5 was evaluated in the U87MG glioblastoma cell line and patient-derived primary GBM cell lines (CG, ZAR, and NULU). Cell viability, migration, and molecular changes were assessed after treatment. Biological activity was also investigated under different pH conditions. Vimentin and phosphorylated ERK (p-ERK) expression were analyzed to investigate the mechanisms underlying sodin 5 activity. Results: Sodin 5 significantly reduced cell viability in all GBM cell lines. Treatment also inhibited cell migration, accompanied by decreased vimentin expression, suggesting cytoskeletal remodeling and reduced invasive potential. Furthermore, sodin 5 decreased p-ERK levels, indicating modulation of signaling pathways involved in proliferation and motility. The protein retained biological activity under different pH conditions, supporting its potential efficacy in the heterogeneous GBM microenvironment. Conclusions: These findings identify sodin 5 as a promising therapeutic candidate for GBM by targeting multiple processes involved in tumor growth and invasion.