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Updated: Jul 7, 2025
Quantitative Immunohistochemistry of the Cellular Microenvironment in Patient Glioblastoma Resections
Published on: July 31, 2017
Role of Glycolytic and Glutamine Metabolism Reprogramming on the Proliferation, Invasion, and Apoptosis Resistance
Cristina Trejo-Solis1, Daniela Silva-Adaya1, Norma Serrano-García1
1Laboratorio Experimental de Enfermedades Neurodegenerativas, Laboratorio de Reprogramación Celular, Departamento de Neurofisiología, Instituto Nacional de Neurología y Neurocirugía, Ciudad de Mexico 14269, Mexico.
Abstract:
Glioma cells exhibit genetic and metabolic alterations that affect the deregulation of several cellular signal transduction pathways, including those related to glucose metabolism. Moreover, oncogenic signaling pathways induce the expression of metabolic genes, increasing the metabolic enzyme activities and thus the critical biosynthetic pathways to generate nucleotides, amino acids, and fatty acids, which provide energy and metabolic intermediates that are essential to accomplish the biosynthetic needs of glioma cells. In this review, we aim to explore how dysregulated metabolic enzymes and their metabolites from primary metabolism pathways in glioblastoma (GBM) such as glycolysis and glutaminolysis modulate anabolic and catabolic metabolic pathways as well as pro-oncogenic signaling and contribute to the formation, survival, growth, and malignancy of glioma cells. Also, we discuss promising therapeutic strategies by targeting the key players in metabolic regulation. Therefore, the knowledge of metabolic reprogramming is necessary to fully understand the biology of malignant gliomas to improve patient survival significantly.
Insights
Glioma cells reprogram metabolism, altering glucose pathways to fuel growth. Targeting these metabolic changes offers new therapeutic strategies for glioblastoma (GBM).
Area of Science:
- Oncology
- Molecular Biology
- Metabolic Pathways
Background:
- Glioma cells display genetic and metabolic changes impacting cellular signaling, particularly glucose metabolism.
- Oncogenic pathways upregulate metabolic genes, boosting enzyme activity for biosynthesis (nucleotides, amino acids, fatty acids).
- These metabolic alterations are crucial for glioma cell energy and biosynthetic requirements.
Purpose of the Study:
- To review how dysregulated metabolic enzymes and metabolites in glioblastoma (GBM) impact primary metabolic pathways like glycolysis and glutaminolysis.
- To explore the modulation of anabolic/catabolic pathways and pro-oncogenic signaling by these metabolic changes.
- To discuss therapeutic strategies targeting key metabolic regulators in glioma.
Main Methods:
- Literature review focusing on metabolic reprogramming in glioblastoma.
- Analysis of primary metabolism pathways (glycolysis, glutaminolysis) and their role in glioma.
- Exploration of oncogenic signaling and its interplay with cellular metabolism.
Main Results:
- Dysregulated metabolic enzymes and metabolites significantly contribute to glioma formation, survival, growth, and malignancy.
- Metabolic reprogramming influences both anabolic and catabolic processes, supporting cancer cell proliferation.
- Targeting metabolic pathways presents a promising therapeutic avenue for GBM treatment.
Conclusions:
- Understanding metabolic reprogramming in malignant gliomas is essential for improving patient outcomes.
- Targeting key metabolic regulators offers potential for novel glioblastoma therapies.
- Metabolic alterations are fundamental to glioma biology and malignancy.
