siRNA沉默PKM2抑制胶质瘤U87细胞的增殖和糖代谢能力  

Silencing PKM2 by siRNA inhibits the proliferation and glucose metabolism of glioma U87 cells

作　　者：王佳甲 陶陶 栾文康 史岩 刘宁 尤永平 

机构地区：[1]南京医科大学第一附属医院神经外科,江苏省210029

出　　处：《江苏医药》2013年第10期1117-1119,共3页Jiangsu Medical Journal

基　　金：国家自然科学基金(81272792);江苏省医学重点人才项目(RC2011051);江苏省医学重点学科(XK201117);江苏省科技厅临床医学科技专项(BL2012028)

摘　　要：目的探讨小分子RNA干扰(siRNA)沉默M2型丙酮酸激酶(PKM2)基因表达对人脑胶质瘤U87细胞增殖和代谢的影响。方法合成PKM2siRNA并转染胶质瘤U87细胞,靶向抑制PKM2表达;将未转染和转染无义siRNA的细胞分别作为空白组和阴性对照组。MTT法检测U87细胞增殖,葡萄糖和乳酸检测试剂盒检测培养基代谢物。结果 PKM2siRNA能有效抑制U87细胞PKM2表达。下调PKM2表达后,细胞增殖能力受到明显抑制,同时葡萄糖消耗量和乳酸生成量也显著下降。结论干扰PKM2表达可显著抑制胶质瘤的增殖和代谢能力,可作为胶质瘤治疗的潜在靶点。Objective To investigate the effects of pyruvate kinase M2 （PKM2） reduction by siRNA on cell proliferation and glucose metabolism of U87 glioma ceils. Methods PKM2 siRNA was transfected into U87 glioma cells, and then PKM2 protein expression was detected by Western blot. Cell proliferation and glucose metabolism were assessed by MTT assay, glucose assay kit and lactate assay kit, respectively. Results Compared to the control groups, PKM2 expression was significantly downregulated in PKM2 siRNA group. Cell proliferation was significantly inhibited 3 days after treatment of PKM2 siRNA PKM2 reduction decreased glucose consumption and lactic acid production. Conclusion Silencing PKM2 by siRNA can effectively inhibit the ability of cell proliferation and glucose metabolism in glioma cells, which can serve as a potential target for glioma therapy.

关 键 词：M2型丙酮酸激酶 小分子RNA干扰 胶质瘤 糖代谢 

分 类 号：R730[医药卫生—肿瘤]