摘要Objective Tumour cells in a hypoxic state are more invasive,have stronger self-renewal capabilities,and are difficult to treat because of their ability to promote tumour recurrence and metastasis.The glycolysis inhibitor 3-bromopyruvic acid(3-BrPA)can completely inactivate glycolytic enzymes at extremely low drug concentrations,thereby exerting a strong inhibitory effect on the glucose energy metabolism of tumor cells.Therefore,we tested the inhibitory effect of 3-BrPA on hepatocellular carcinoma cells(HepG2)in vitro;then,we used the VX2 liver cancer model to study the antitumour effect of 3-BrPA combined with interventional embolization on liver cancer.Methods In vitro,a CCK-8 assay was used to detect the inhibitory effect of different concentrations of 3-BrPA on HepG2 cells,and light microscopy confirmed that the HepG2 cells were completely dead.Western blotting was used to detect the expression of key proteins involved in apoptosis.A total of 30 New Zealand white rabbits were used to establish a liver cancer model and were randomly divided into 3 groups 2 weeks after tumor establishment:the control group was perfused with saline in the hepatic artery;the transcatheter arterial embolization(TAE)group was given TAE;and the experimental group was perfused with 3-BrPA combined with TAE.The tumor-bearing rabbits were killed one week after surgery.The tumor volume and tumor necrosis ratio were calculated via the histopathological examination.Results In vitro,the inhibitory effect of 3-BrPA on HepG2 cells increased with increasing concentration.3-BrPA(100 μmol/L)could induce the necrosis of HepG2 cells.Stimulation with 50 μmol/L 3-BrPA could activate the tumor cell apoptosis pathway.3-BrPA combined with TAE treatment could significantly inhibit tumor growth and cause more complete tumor necrosis.Conclusion 3-BrPA not only has antitumour effects in vitro but can also significantly improve antitumour effects in the hypoxic microenvironment after embolization in vivo.