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Role of Energy Metabolism in the Progression of Neuroblastoma

Journal

Publisher

MDPI
DOI: 10.3390/ijms222111421

Keywords

neuroblastoma; glycolysis; extracellular vesicles

Funding

  1. Medical University of Gdansk grants: Excellence Initiative-Research University [IDUB 664/249/61/71-1409, 02-00904//07/643]

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Neuroblastoma is a common childhood cancer with a significant risk of death. Recent studies have shown that extracellular vesicles play a crucial role in promoting tumorigenesis by carrying metabolic enzymes that influence energy metabolism. Glycolysis has been identified as playing a primary role in energy metabolism in neuroblastoma.
Neuroblastoma is a common childhood cancer possessing a significant risk of death. This solid tumor manifests variable clinical behaviors ranging from spontaneous regression to widespread metastatic disease. The lack of promising treatments calls for new research approaches which can enhance the understanding of the molecular background of neuroblastoma. The high proliferation of malignant neuroblastoma cells requires efficient energy metabolism. Thus, we focus our attention on energy pathways and their role in neuroblastoma tumorigenesis. Recent studies suggest that neuroblastoma-driven extracellular vesicles stimulate tumorigenesis inside the recipient cells. Furthermore, proteomic studies have demonstrated extracellular vesicles (EVs) to cargo metabolic enzymes needed to build up a fully operative energy metabolism network. The majority of EV-derived enzymes comes from glycolysis, while other metabolic enzymes have a fatty acid beta-oxidation and tricarboxylic acid cycle origin. The previously mentioned glycolysis has been shown to play a primary role in neuroblastoma energy metabolism. Therefore, another way to modify the energy metabolism in neuroblastoma is linked with genetic alterations resulting in the decreased activity of some tricarboxylic acid cycle enzymes and enhanced glycolysis. This metabolic shift enables malignant cells to cope with increasing metabolic stress, nutrition breakdown and an upregulated proliferation ratio.

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