Knock-down of PGM1 inhibits cell viability, glycolysis, and oxidative phosphorylation in glioma under low glucose condition via the Myc signaling pathway.

PGM1 is an essential enzyme for glucose metabolism and is involved in cell viability, proliferation, and metabolism. However, the regulatory role of PGMI in glioma progression and the relation between gliomas and PGM1 expression are still unclear. This study aimed to explore the role of PGM1 in glycolysis and oxidative phosphorylation in glioma. Correlation and enrichment analyses of PGM1 in glioma cells were explored in TCGA database and two hospital cohorts. The cell viability, glycolysis, and oxidative phosphorylation were investigated in PGM1 knock-down and overexpression situations. Higher PGM1 expression in glioma patients was associated with a poor survival rate. However, knock-down of PGM1 reduced glioma cell viability, glycolysis, and oxidative phosphorylation under low glucose condition. Moreover, it suppressed tumor growth in vivo. On the other hand, PGM1 overexpression promoted glioma cell viability, glycolysis, and oxidative phosphorylation under low glucose condition by a Myc positive feedback loop. Glioma patients with higher PGM1 expression were associated with poor survival rates. Additionally, PGM1 could promote glioma cell viability, glycolysis, and oxidative phosphorylation under low glucose condition via a myc-positive feedback loop, suggesting PGM1 could be a potential therapeutic target for gliomas.