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Volume 15
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10.3390/brainsci15080884
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Review

Redox-Regulated Pathways in Glioblastoma Stem-like Cells: Mechanistic Insights and Therapeutic Implications

by
Nadia Fernanda Esteban-Román
1,†,
Elisa Taddei
2,†,
Edson Castro-Velázquez
3,
Lorna Villafuentes-Vidal
4,
Alejandra Velez-Herrera
5,
Moisés Rubio-Osornio
6 and
Carmen Rubio
2,*
1
Faculty of Veterinary Medicine, Universidad Autónoma Metropolitana, Mexico City 04960, Mexico
2
Department of Neurophysiology, Instituto Nacional de Neurología y Neurocirugía, Mexico City 14269, Mexico
3
Faculty of Medicine, University of Guadalajara, Guadalajara 44340, Mexico
4
Mexican Faculty of Medicine, Universidad La Salle, Mexico City 14000, Mexico
5
University Center for Health Sciences, University of Guadalajara, Guadalajara 44340, Mexico
6
Department of Neurochemistry, Instituto Nacional de Neurología y Neurocirugía, Mexico City 14269, Mexico
*
Author to whom correspondence should be addressed.
†
These authors contributed equally to this work.
Brain Sci. 2025, 15(8), 884; https://doi.org/10.3390/brainsci15080884
Submission received: 14 July 2025 / Revised: 9 August 2025 / Accepted: 13 August 2025 / Published: 19 August 2025
(This article belongs to the Section Neuro-oncology)
Review Reports Versions Notes

Abstract

Glioblastoma (GBM) is the most aggressive primary brain tumor, characterized by rapid proliferation, invasiveness, therapeutic resistance, and an immunosuppressive tumor microenvironment. A subpopulation of glial stem-like cells (GSCs) within GBM tumors contributes significantly to tumor initiation, progression, and relapse, displaying remarkable adaptability to oxidative stress and metabolic reprogramming. Recent evidence implicates the atypical kinases RIOK1 and RIOK2 in promoting GBM growth and proliferation through their interaction with oncogenic pathways such as AKT and c-Myc. Concurrently, the redox-sensitive Nrf2/Keap1 axis regulates antioxidant defenses and supports GSC survival and chemoresistance. Additionally, aberrant activation of the canonical Wnt/β-catenin pathway in GSCs enhances their self-renewal, immune evasion, and resistance to standard therapies, particularly under oxidative stress conditions. This review integrates current knowledge on how redox homeostasis and key signaling pathways converge to sustain GSC maintenance and GBM malignancy. Finally, we discuss emerging redox-based therapeutic strategies designed to target GSC resilience, modulate the tumor immune microenvironment, and surmount treatment resistance.
Keywords: glial stem-like cells; glioma; glioblastoma; oxidative stress; redox-targeted therapy; cancer stem cells glial stem-like cells; glioma; glioblastoma; oxidative stress; redox-targeted therapy; cancer stem cells

Share and Cite

MDPI and ACS Style

Esteban-Román, N.F.; Taddei, E.; Castro-Velázquez, E.; Villafuentes-Vidal, L.; Velez-Herrera, A.; Rubio-Osornio, M.; Rubio, C. Redox-Regulated Pathways in Glioblastoma Stem-like Cells: Mechanistic Insights and Therapeutic Implications. Brain Sci. 2025, 15, 884. https://doi.org/10.3390/brainsci15080884

AMA Style

Esteban-Román NF, Taddei E, Castro-Velázquez E, Villafuentes-Vidal L, Velez-Herrera A, Rubio-Osornio M, Rubio C. Redox-Regulated Pathways in Glioblastoma Stem-like Cells: Mechanistic Insights and Therapeutic Implications. Brain Sciences. 2025; 15(8):884. https://doi.org/10.3390/brainsci15080884

Chicago/Turabian Style

Esteban-Román, Nadia Fernanda, Elisa Taddei, Edson Castro-Velázquez, Lorna Villafuentes-Vidal, Alejandra Velez-Herrera, Moisés Rubio-Osornio, and Carmen Rubio. 2025. "Redox-Regulated Pathways in Glioblastoma Stem-like Cells: Mechanistic Insights and Therapeutic Implications" Brain Sciences 15, no. 8: 884. https://doi.org/10.3390/brainsci15080884

APA Style

Esteban-Román, N. F., Taddei, E., Castro-Velázquez, E., Villafuentes-Vidal, L., Velez-Herrera, A., Rubio-Osornio, M., & Rubio, C. (2025). Redox-Regulated Pathways in Glioblastoma Stem-like Cells: Mechanistic Insights and Therapeutic Implications. Brain Sciences, 15(8), 884. https://doi.org/10.3390/brainsci15080884

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