Effect Of EGF Activating PI3K/AKT Pathways On Esophageal Carcinoma HIF-1α Silencing And Carcinoma Cell Glycolysis

Objective：To study whether hypoxia-inducible factor-1α (HIF-1α) is necessary forenhancing glycolysis of esophageal carcinoma cells and whether thereis a HIF-1α non-dependent regulation mechanism for activation ofPI3K/AKT pathways to improve glycolysis.Methods: Eca109and siHIF-Eca109esophageal carcinoma cell lines are culturedin vitro. After epidermal growth factors (EGF) are added to promoteactivation of PI3K/AKT pathways, the PT-PCR method is applied todetermining the level of HIF-1α and rate-limiting enzyme mRNA, theWestern blot method to determining the protein expression of HIF-1αand rate-limiting enzyme in glycolysis, and the spectrophotometricmethod to determining the lactate concentration in cultured supernate.Results: In siHIF-Eca109cell lines, the expression of hexokinase-II (HK-II),phosphofructokinase-2(PFK-2), lactate dehydrogenase A (LDHA) andglucose carrier protein-1(GLUT1) is suppressed with HIF-1α silencing(P0.01), but no significant difference is observed after EGF added foractivation (P0.05). The lactate is much less secreted after HIF-1αsilencing (P0.01), but no significant difference is found after EGF addedfor activation (P0.05). Conclusion: HIF-1α silencing significantly reduces glycolysis of esophagealcarcinoma cells, which cannot be corrected by EGF activatingPI3K/AKT pathways. Therefore, HIF-1α is indispensable forenhancing glycolysis of esophageal carcinoma cells.