Targeting Glioblastoma Metabolism
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".
Deadline for manuscript submissions: 10 June 2025 | Viewed by 3249
Special Issue Editors
2. Instituto de Investigación Biomédica de Málaga (IBIMA), 29010 Málaga, Spain
Interests: cancer mitochondrial metabolism; oxidative stress; tumor-specific isoenzymes; combined therapies against cancer
Special Issues, Collections and Topics in MDPI journals
Interests: cancer omics; cancer metabolic reprogramming; tumor nitrogen metabolism; structure-function studies; drug design
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Glioblastoma is one of the most lethal forms of cancer, characterized by its high degree of malignancy and resistance to conventional treatments. Two key features that make glioblastoma particularly devastating are their extensive infiltration into surrounding brain tissue and the presence of heterogeneous populations of highly aggressive cancer stem cells. These cancer stem cells are notoriously resistant to standard therapies, and their ability to evade treatment leads to recurrent tumors with fatal consequences for patients.
A major contributing factor to glioblastoma's resistance to treatment is the metabolic heterogeneity and plasticity exhibited by the tumor cells. These metabolic alterations play a critical role in tumor progression and are closely tied to the development of therapeutic resistance. Such metabolic variability makes it exceedingly difficult to establish a universal therapy, not only across different cancer types but also within subtypes of the same cancer, and even for individual patients throughout their disease progression. Cancer metabolism evolves as the tumor develops, with substantial changes occurring during the initiation, progression, and metastasis of the disease. This dynamic metabolic landscape presents both challenges and opportunities for therapeutic intervention. Identifying metabolic vulnerabilities in the early (preneoplastic) stages as well as during the active and metastatic phases is crucial for slowing tumor progression and preventing fatal outcomes. Moreover, the metabolic changes occurring in tumor cells also affect the surrounding tumor microenvironment, which further complicates therapeutic strategies.
In the context of glioblastoma, targeting specific metabolic pathways represents a promising approach to therapy. One critical area of investigation involves the targeting of the metabolic consequences of the IDH1/2 mutations, which are commonly found in glioblastoma. These mutations lead to the production of (R)-2-hydroxyglutarate, a metabolite that functions as an oncometabolite, contributing to both tumorigenesis and resistance to conventional treatments. The accumulation of (R)-2-hydroxyglutarate disrupts normal cellular processes, including epigenetic regulation, which may further promote tumor growth and metastasis. Consequently, targeting the IDH1/2 mutation and its associated metabolic effects could provide a means to hinder tumor progression.
Additionally, there is growing evidence that nitrogen metabolism plays a significant role in the reprogramming of glioblastoma cells. Alterations in nitrogen metabolism could impact various cellular processes, including protein synthesis, energy production, and the maintenance of cellular redox balance. Understanding the intricate details of nitrogen metabolism in glioblastoma cells and its interaction with key metabolic enzymes is essential for developing novel therapeutic strategies to disrupt these pathways.
Furthermore, it is increasingly recognized that epigenetic regulation is a critical factor in glioblastoma metabolism. Epigenetic modifications, such as DNA methylation and histone modifications, can significantly influence the expression of metabolic genes, contributing to the tumor’s ability to adapt to various stresses and therapeutic interventions. Therefore, it is vital to investigate how epigenetic alterations affect metabolic pathways in glioblastoma, and how these changes can be targeted to reduce the malignancy and aggressiveness of the tumor.
In conclusion, understanding the complex interplay between metabolic reprogramming, genetic mutations, and epigenetic regulation in glioblastoma is crucial for developing more effective therapies. By focusing on the metabolic vulnerabilities of glioblastoma cells, particularly those driven by mutations like IDH1/2 and the reprogramming of nitrogen metabolism, we may be able to devise targeted interventions that not only slow tumor progression but also overcome the resistance mechanisms that make glioblastoma so difficult to treat.
This Special Issue, Glioblastoma Metabolism, will contain experimental papers, but up-to-date reviews are welcome.
Prof. Dr. José M. Matés
Dr. José Ángel Campos Sandoval
Guest Editors
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Keywords
- glioblastoma
- metabolic heterogeneity
- metabolic reprogramming
- cancer stem cells
- therapeutic resistance
- metabolic vulnerabilities
- IDH1/2 mutations
- tumor microenvironment
- epigenetic regulation
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