Tumor metabolism characterized by aerobic glycolysis makes the Warburg effect a unique target for
tumor therapy. Recent studies have found that
glycogen branching enzyme 1 (GBE1) is involved in
cancer progression. However, the study of GBE1 in
gliomas is limited. We determined by bioinformatics analysis that GBE1 expression is elevated in
gliomas and correlates with poor prognoses. In vitro experiments showed that GBE1 knockdown slows
glioma cell proliferation, inhibits multiple
biological behaviors, and alters
glioma cell glycolytic capacity. Furthermore, GBE1 knockdown resulted in the inhibition of the NF-κB pathway as well as elevated expression of
fructose-bisphosphatase 1 (FBP1). Further knockdown of elevated FBP1 reversed the inhibitory effect of GBE1 knockdown, restoring glycolytic reserve capacity. Furthermore, GBE1 knockdown suppressed xenograft
tumor formation in vivo and conferred a significant survival benefit. Collectively, GBE1 reduces FBP1 expression through the NF-κB pathway, shifting the
glucose metabolism pattern of
glioma cells to glycolysis and enhancing the Warburg effect to drive
glioma progression. These results suggest that GBE1 can be a novel target for
glioma in metabolic
therapy.