摘要 : We investigated the regulatory effects of hypoxia-inducible factor-1 alpha (HIF-1 alpha) on glycolysis metabolism in esophageal carcinoma (ESCA) cells. A series of bioinformatics databases and tools were used to investigate the ex... 展开 We investigated the regulatory effects of hypoxia-inducible factor-1 alpha (HIF-1 alpha) on glycolysis metabolism in esophageal carcinoma (ESCA) cells. A series of bioinformatics databases and tools were used to investigate the expression and role of HIF-1 alpha in ESCA. The expression of HIF-1 alpha in ESCA tissues and adjacent tissues was validated by real-time PCR. Small interfering RNA (siRNA) was used to inhibit HIF-1 alpha-related genes in human ESCA cells (Eca109 and KYSE150). Cell proliferation was detected by the CCK-8 assay. The expression of HIF-1 alpha and glycolytic enzymes were investigated by real-time PCR and Western blot. HIF-1 alpha is highly expressed in ESCA and is involved in many biological processes such as cell hypoxia reaction, glucose metabolic process. Further in vitro experiments showed that expression of HIF-1 alpha in Eca109 and KYSE150 significantly increased under hypoxia compared with normoxia conditions. Also, the glucose uptake and lactate production under hypoxia were higher. The expression levels of hexokinase 2 (HK2) and pyruvate dehydrogenase kinase 1 (PDK1), glycolysis-related genes, were significantly increased under hypoxia. After siRNA knockdown of HIF-1 alpha in Eca109 and KYSE150, the glucose uptake and lactate production, as well as cell proliferation were significantly decreased under hypoxia, and HK2 and PDK1 were significantly downregulated. HIF-1 alpha promotes glycolysis of ESCA cells by upregulating the expression of HK2 and PDK1 under hypoxia. 收起