ArticleTranslational cancer research2025
5MPN effectively targets PFKFB4 and inhibits the glucose metabolism process and invasion of glioblastoma.
Article in Translational cancer research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Gliomas are the most common malignant tumors of the central nervous system, with glioblastoma multiforme (GBM) being the most aggressive and having the poorest prognosis. Although there are few targeted therapies available, the glucose metabolism of GBM, characterized by aerobic glycolysis, presents a potential therapeutic target. While many studies have focused on glucose metabolism in GBM, research on phosphofructokinase-2/fructose-2,6-bisphosphatase 4 (PFKFB4), a key regulatory kinase, remains limited. This study aims to investigate the inhibitory effects of targeting PFKFB4 in GBM and explore its molecular mechanisms. Methods: In this study, we analyzed the expression levels of PFKFB4, its correlation with prognosis, and its relationship with other genes using The Cancer Genome Atlas (TCGA) and Chinese Glioma Genome Atlas (CGGA) datasets. We also selected 5MPN (a specific PFKFB4 inhibitor not yet studied in GBM) as the focus of our experiments, evaluating its impact on glucose metabolism and invasiveness in GBM cells. Results: Our study found that PFKFB4 is highly expressed in GBM and correlates with poor prognosis. 5MPN [half-maximal inhibitory concentration (IC50) of 14.62 µM in U251 cells and 10.15 µM in T98 cells] effectively inhibits glycolysis (at 5 µM) and invasiveness (at 2 µM) in GBM cells. We also explored potential molecular mechanisms that may work synergistically with PFKFB4, supported by data from public databases. Conclusions: PFKFB4 shows therapeutic potential as a target for GBM treatment, and its inhibitor 5MPN significantly inhibits glycolysis and invasiveness in GBM. This study provides new insights and potential drug options for targeted therapy in GBM.
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