Moreover, FH535 exhibited a significant inhibitory effect on the promotion of basal glycolysis and glycolytic capacity induced by HMGB3 overexpression, as shown in Fig. 6D. Additionally, FH535 partially attenuated the upregulation of glycolytic marker proteins resulting from HMGB3 overexpression, as evidenced in Fig. 6E. In summary, these findings demonstrate that the overexpression of HMGB3 promotes glycolysis in cancer cells, which is attributed to the activation of the Wnt/β-catenin pathway. This evidence concerns the gene HMGB3 and cancer.