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Peer-reviewedCC BYToxins

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

  • Veronica Russo1
  • Sara Ragucci2
  • Miriam Russo1
  • Maria Antonietta Oliva1
  • Nicola Landi2,3
  • Antimo Di Maro2
  • Antonietta Arcella1
  1. 1IRCCS Istituto Neurologico Mediterraneo NEUROMED, Via Atinense 18, 86077 Pozzilli, IS, Italy.
  2. 2Department of Environmental, Biological and Pharmaceutical Sciences and Technologies (DiSTABiF), University of Campania "Luigi Vanvitelli", Via Vivaldi 43, 81100 Caserta, CE, Italy.
  3. 3Institute of Crystallography, National Research Council, Via Vivaldi 43, 81100 Caserta, CE, Italy.
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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.

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Cite

BibTeXRIS
BibTeX
@article{russo2026effects,
  title = {{Effects of Sodin 5 on the Proliferation and Migration of Human Glioblastoma Cells.}},
  author = {Veronica Russo and Sara Ragucci and Miriam Russo and Maria Antonietta Oliva and Nicola Landi and Antimo Di Maro and Antonietta Arcella},
  journal = {Toxins},
  year = {2026},
  month = oct,
  doi = {10.3390/toxins18100441},
  url = {https://europepmc.org/article/MED/42931532},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Effects of Sodin 5 on the Proliferation and Migration of Human Glioblastoma Cells.
AU  - Veronica Russo
AU  - Sara Ragucci
AU  - Miriam Russo
AU  - Maria Antonietta Oliva
AU  - Nicola Landi
AU  - Antimo Di Maro
AU  - Antonietta Arcella
PY  - 2026
DA  - 2026/10/13
JO  - Toxins
DO  - 10.3390/toxins18100441
UR  - https://europepmc.org/article/MED/42931532
AB  - 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.
SN  - 2072-6651
ER  -