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    宋虎, 徐溢新, 许腾, 樊瑞智, 曹猛, 徐为, 宋军. Lin28A过表达对结肠癌细胞糖酵解的促进作用及其机制[J]. 徐州医科大学学报, 2017, 37(12): 773-775.
    引用本文: 宋虎, 徐溢新, 许腾, 樊瑞智, 曹猛, 徐为, 宋军. Lin28A过表达对结肠癌细胞糖酵解的促进作用及其机制[J]. 徐州医科大学学报, 2017, 37(12): 773-775.
    SONG Hu, XU Yixin, XU Teng, FAN Ruizhi, CAO Meng, XU Wei, SONG Jun. Effects of Lin28A over-expression on the glycosis of colon cancer cells[J]. Journal of Xuzhou Medical University, 2017, 37(12): 773-775.
    Citation: SONG Hu, XU Yixin, XU Teng, FAN Ruizhi, CAO Meng, XU Wei, SONG Jun. Effects of Lin28A over-expression on the glycosis of colon cancer cells[J]. Journal of Xuzhou Medical University, 2017, 37(12): 773-775.

    Lin28A过表达对结肠癌细胞糖酵解的促进作用及其机制

    Effects of Lin28A over-expression on the glycosis of colon cancer cells

    • 摘要: 目的探讨Lin28A基因过表达后对结肠癌细胞葡萄糖代谢的影响及相关分子机制。方法利用慢病毒载体建立Lin28A过表达结肠癌HT-29细胞株,以生化法检测细胞培养液乳酸含量,ELISA法检测细胞内磷酸果糖(PFK)含量,蛋白质印迹法检测Lin28A、Lin28A、缺氧诱导因子-1α(HIF-1α)、葡萄糖转运蛋白-1(GLUT-1)、丙酮酸激酶M2( PKM2)蛋白水平表达。结果Lin28A在结肠癌细胞过表达后蛋白水平明显升高,而let-7a表达降低;细胞培养液乳酸含量和细胞内PFK含量均升高;糖代谢相关蛋白HIF-1α、GLUT-1、PKM2水平明显升高。结论Lin28A过表达可以促进结肠癌细胞的糖酵解,其作用机制可能通过上调HIF-1α、GLUT-1、PKM2水平而实现。

       

      Abstract: ObjectiveTo explore the effects of Lin28A over-expression on the glycolysis of colon cancer cells. MethodsLin28A was over-expressed in colon cancer HT-29 cells using lentiviral vectors. The amount of lactic acid in the culture media was measured by biological methods. The level of phosphate fructose kinase (PFK) in the cells was also detected by ELISA. The levels of Lin28A, hypoxia inducible factor-1α (HIF-1α), glucose transporter 1 (GLUT-1), and pyruvate kinase M2 (PKM2) were detected using Western blotting. ResultsOver-expression of Lin28A in colon cancer cells resulted in increases in its protein levels but decreases in expression of let-7a. Over-expression of Lin28A also up-regulated the level of lactic acid in the culture media and PFK levels in the cells, as well as the expression of HIF-1α, GLUT-1, and PKM2. ConclusionsOver-expression of Lin28A promotes the glycolysis of colon cancer cells, which may be related with the up-regulation of HIF-1α, GLUT-1, and PKM2.

       

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