Fubp1 supports the lactate-Akt-mTOR axis through the upregulation of Hk1 and Hk2

Cells require energy for homeostatic activities, growth and division. By utilizing glucose as the main energy source, cells generate ATP and metabolic precursors through glycolysis and citric acid cycle. Although the oxidative phosphorylation can produce more ATP molecules from one molecule of glucose than glycolysis, rapidly growing cells primarily metabolize glucose via aerobic glycolysis. This aerobic glycolysis makes cells to uptake glucose at a higher rate and to efficiently convert glucose into the macromolecules required for new daughter cells. Recent evidence suggests that Fubp1 promotes cell proliferation and survival, and it is overexpressed in a variety of cancers. However, the role of Fubp1 in cellular metabolism remains unclear. In the present study, we demonstrated that Fubp1 upregulates the mRNA levels of two hexokinase genes, Hk1 and Hk2. We also found the positive correlation in mRNA expression between Fubp1 and both of hexokinase genes in several types of cancers. We suggest that Fubp1 contributes to cell survival through supporting lactate-Akt-mTOR axis. •Transcriptional profiling reveals the enrichment of Fubp1 in several types of tumors.•Fubp1 contributes to the lactate production by upregulation of Hk1 and Hk2.•There is a positive correlation between the expression of Fubp1 and hexokinase genes.•Fubp1 deficiency decreased cell survival through downregulating Akt-mTOR axis.