Butein Inhibited In Vitro Hexokinase-2-Mediated Tumor Glycolysis in Hepatocellular Carcinoma by Blocking Epidermal Growth Factor Receptor (EGFR)

• Published in: Medical science monitor 2018-05, Vol.24, p.3283-3292
• Main Authors: Liao, Weirong, Liu, Jingtian, Zhang, Dawei, Huang, Wenhai, Chen, Runhao
• Format: Article
• Language: English
• Subjects: Apoptosis - drug effects; Carcinoma, Hepatocellular - metabolism; Carcinoma, Hepatocellular - pathology; Cell Line, Tumor; Cell Proliferation - drug effects; Chalcones - pharmacology; Glycolysis - drug effects; Hexokinase - metabolism; Humans; Lab/In Vitro Research; Liver Neoplasms - metabolism; Liver Neoplasms - pathology; Receptor, Epidermal Growth Factor - metabolism; Signal Transduction - drug effects
• ISSN: 1643-3750; 1234-1010; 1643-3750
• DOI: 10.12659/MSM.906528

BACKGROUND Anaerobic glycolysis is an important physiological process of all cancer cells. Butein has been reported to demonstrate substantial antitumor activities in various cancers. However, the effect of butein on tumor glycolysis remains unclear. In this study, the effect of butein on tumor glycolysis and the underlying mechanism were investigated in hepatocellular carcinoma (HCC). MATERIAL AND METHODS Cell proliferation assay and anchorage-independent growth assay were carried out to evaluate the antitumor activities of butein in vitro. The effect of butein on tumor glycolysis was determined by examining the changes in glucose uptake and lactate production. Hexokinase-2 (HK-2) expression in HCC cells upon butein treatment was analyzed by Western blotting. The activity of butein on EGFR signaling pathway was studied and its potency in EGFR exogenous overexpression cells was investigated. RESULTS After butein treatment, HCC cell proliferation was significantly inhibited (91.4% in Hep3B and 88.2% in Huh-7 at 80 μM, p