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Peer-reviewedCC BY 4.0Oncology Research

Hexokinases and Glial Tumor Metabolism: A Bridge between Bioenergetics and Translational Oncology

  • Corina Ionela Tamas1,2
  • Flaviu Tamas1,2
  • Alina Roxana Cehan3
  • Adrian Balasa1,2
  1. 1Department of Neurosurgery, “George Emil Palade” University of Medicine, Pharmacy, Science and Technology, Targu Mures, Romania
  2. 2Department of Neurosurgery, Emergency Clinical County Hospital, Targu Mures, Romania
  3. 3Doctoral School of Medicine and Pharmacy, “George Emil Palade” University of Medicine, Pharmacy, Science and Technology, Targu Mures, Romania
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Abstract

Hexokinases, particularly hexokinase 2, play a central role in the metabolic reprogramming of glioblastoma and other malignant glial tumors by promoting aerobic glycolysis and sustaining the Warburg phenotype. This review aims to summarize the current evidence regarding the molecular regulation, biological significance, and therapeutic implications of hexokinase isoenzymes in glial tumor metabolism. Recent studies consistently demonstrate that hexokinase 2 overexpression is associated with enhanced tumor proliferation, invasiveness, angiogenesis, resistance to chemotherapy and radiotherapy, and poor prognosis, especially in glioblastoma and high-grade gliomas. Multiple regulatory mechanisms, including microRNAs, long non-coding RNAs, the phosphatidylinositol 3-kinase/protein kinase B signaling pathway, and hypoxia-inducible factor 1-alpha-mediated signaling, as well as mitochondrial interactions through the voltage-dependent anion channel, contribute to metabolic adaptation and tumor progression. In addition to its metabolic role, hexokinase 2 has emerged as an important mediator of the immunosuppressive tumor microenvironment and maintenance of the malignant phenotype. Overall, targeting hexokinase 2 and related glycolytic pathways represents a promising strategy for personalized metabolic therapy and may improve responsiveness to conventional oncologic treatments in patients with gliomas.

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Cite

BibTeXRIS
BibTeX
@article{tamas2026hexokinases,
  title = {{Hexokinases and Glial Tumor Metabolism: A Bridge between Bioenergetics and Translational Oncology}},
  author = {Corina Ionela Tamas and Flaviu Tamas and Alina Roxana Cehan and Adrian Balasa},
  journal = {Oncology Research},
  year = {2026},
  month = oct,
  doi = {10.32604/or.2026.079467},
  url = {https://doi.org/10.32604/or.2026.079467},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Hexokinases and Glial Tumor Metabolism: A Bridge between Bioenergetics and Translational Oncology
AU  - Corina Ionela Tamas
AU  - Flaviu Tamas
AU  - Alina Roxana Cehan
AU  - Adrian Balasa
PY  - 2026
DA  - 2026/10/28
JO  - Oncology Research
DO  - 10.32604/or.2026.079467
UR  - https://doi.org/10.32604/or.2026.079467
AB  - Hexokinases, particularly hexokinase 2, play a central role in the metabolic reprogramming of glioblastoma and other malignant glial tumors by promoting aerobic glycolysis and sustaining the Warburg phenotype. This review aims to summarize the current evidence regarding the molecular regulation, biological significance, and therapeutic implications of hexokinase isoenzymes in glial tumor metabolism. Recent studies consistently demonstrate that hexokinase 2 overexpression is associated with enhanced tumor proliferation, invasiveness, angiogenesis, resistance to chemotherapy and radiotherapy, and poor prognosis, especially in glioblastoma and high-grade gliomas. Multiple regulatory mechanisms, including microRNAs, long non-coding RNAs, the phosphatidylinositol 3-kinase/protein kinase B signaling pathway, and hypoxia-inducible factor 1-alpha-mediated signaling, as well as mitochondrial interactions through the voltage-dependent anion channel, contribute to metabolic adaptation and tumor progression. In addition to its metabolic role, hexokinase 2 has emerged as an important mediator of the immunosuppressive tumor microenvironment and maintenance of the malignant phenotype. Overall, targeting hexokinase 2 and related glycolytic pathways represents a promising strategy for personalized metabolic therapy and may improve responsiveness to conventional oncologic treatments in patients with gliomas.
SN  - 0965-0407
SN  - 1555-3906
ER  -