Albendazole inhibits HIF-1 alpha-dependent glycolysis and VEGF expression in non-small cell lung cancer cells

作者：Zhou, Fang^*; Du, Jin; Wang, Jianjun

来源：Molecular and Cellular Biochemistry, 2017, 428(1-2): 171-178.

DOI：10.1007/s11010-016-2927-3

• Albendazole
• HIF-1 alpha
• Glycolysis
• VEGF
• Non-small cell lung cancer

Albendazole (ABZ) has an anti-tumor ability and inhibits HIF-1 alpha activity. HIF-1 alpha is associated with glycolysis and vascular endothelial cell growth factor (VEGF) expression, which plays an important role in cancer progression. These clues indicate that ABZ exerts an anti-cancer effect by regulating glycolysis and VEGF expression. The aim of this study is to clarify the effects of ABZ on non-small cell lung cancer (NSCLC) cells and explore the underlying molecular mechanisms. The expression levels of HIF-1 alpha and VEGF were detected using western blot analysis, and the effect of ABZ on glycolysis was evaluated by measuring the relative activities of hexokinase (HK), pyruvate kinase (PK), and lactate dehydrogenase (LDH) and detecting the production of lactate in A549 and H1299 cells. The results showed that ABZ decreased the expression levels of HIF-1 alpha and VEGF and suppressed glycolysis in under hypoxia, but not normoxic condition. Inhibiting HIF-1 alpha also suppressed glycolysis and VEGF expression. Additionally, ABZ inhibited the volume and weight, decreased the relative activities of HK, PK, and LDH, and reduced the levels of HIF-1 alpha and VEGF of A549 xenografts in mouse models. In conclusion, ABZ inhibited growth of NSCLC cells by suppressing HIF-1 alpha-dependent glycolysis and VEGF expression.

• 出版日期2017-4
• 单位河南大学