Abstract
Glioma is the most common tumor with the worst prognosis in the central nervous system. Current studies showed that glucose metabolism could affect the malignant progression of tumors. However, the study on the dysregulation of glucose metabolism in glioma is still limited. Herein, we firstly screened 48 differentially expressed glucose metabolism-related genes (DE-GMGs) by comparing glioblastomas to low-grade gliomas. Then a glucose metabolism-related gene (GMG)-based model (PC, lactate dehydrogenase A (LDHA), glucuronidase beta (GUSB), galactosidase beta 1 (GLB1), galactose mutarotase (GALM), or fructose-bisphosphatase 1 (FBP1)) was constructed by a protein–protein interaction (PPI) network and Lasso regression. Thereinto, the high-risk group encountered a worse prognosis than the low-risk group, and the M2 macrophage was positively relevant to the risk score. Various classical tumor-related functions were enriched by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses. Since protein GALM was rarely studied in glioma, we detected high expression of GALM by western blot and immunohistochemistry in glioma tissues. And experiments in vitro showed that GALM could promote the epithelial-to-mesenchymal transition (EMT) process of glioma cells and could be regulated by TNFAIP3 in glioma cells. Overall, our study revealed the critical role of glucose metabolism in the prognosis of patients with glioma. Furthermore, we demonstrated that GALM was significantly related to the malignancy of glioma and could promote glioma cells’ EMT process.
Highlights
Glioma is a common intracranial tumor with high mortality and morbidity (Ostrom et al, 2014)
Speaking, in the field of neuro-oncology, significant progress has been made in metabonomics, the study on how brain tumors reprogram metabolic pathways is still limited (Venneti and Thompson, 2017)
The reprogramming of glucose metabolism is a promising strategy for the treatment of gliomas (Lu et al, 2020)
Summary
Glioma is a common intracranial tumor with high mortality and morbidity (Ostrom et al, 2014). Recent studies have found that the metabolic reprogramming of tumors could replace the normal metabolic pathway, support the growth and proliferation of cells, and meet the associated bioenergetic and biosynthetic demands (Hanahan and Weinberg, 2011). Studies reported that tumor cells reprogram glucose metabolism and promote tumor growth, proliferation, invasion, and drug resistance through the Warburg effect (Vander Heiden et al, 2009; Liberti and Locasale, 2016; Icard et al, 2018). The current treatments may be improved by affecting cellular glucose metabolism (Woolf and Scheck, 2015). Many studies have found pathways that affect glucose metabolism in glioma cells; for example, p53 could combine with oncogenes to drive glucose metabolism in glioblastomas (GBMs) (Mai et al, 2017). Understanding the changes in glucose metabolism of gliomas would provide a new strategy for cancer treatment (DeBerardinis and Chandel, 2016)
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