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作 者:柴双[1] 卞齐龙 于涛[1] 欧阳仲瑞 赵海杞 刘珈杞 侯旭[1] 赵世光[1] 刘耀华[1]
机构地区:[1]哈尔滨医科大学附属第一医院神经外科,哈尔滨市150001
出 处:《中国肿瘤临床》2016年第20期892-897,共6页Chinese Journal of Clinical Oncology
基 金:国家自然科学基金项目(编号:81372701)资助~~
摘 要:目的:明确低氧应激对胶质瘤细胞X-盒结合蛋白1(X-box binding protein 1,XBP1)的作用;明确胶质瘤细胞XBP1表达与糖代谢之间的关系;抑制XBP1表达对胶质瘤细胞在常氧和低氧环境下细胞活力的影响;明确低氧环境中XBP1对胶质瘤细胞糖酵解的影响。方法:分别在常氧和低氧条件下培养人脑胶质瘤细胞系,检测XBP1激活情况;使用si RNA技术抑制XBP1表达,使用氧化磷酸化抑制剂处理细胞,检测细胞活力及糖代谢方式的改变,在常氧和低氧条件下检测细胞存活及糖酵解产物。结果:低氧环境下XBP1活化增加。低氧环境下XBP1沉默降低胶质瘤细胞活力、ATP和乳酸生成,葡萄糖消耗量减少。细胞氧化磷酸化受到抑制后,XBP1沉默降低胶质瘤细胞存活率。结论:低氧环境可诱导胶质瘤细胞XBP1的活化。在低氧环境下XBP1沉默降低胶质瘤细胞活力和糖酵解,胶质瘤细胞的糖酵解依赖于XBP1活化。Objective:To determine the effect of hypoxic stress on glioma cell XBP1 expression, the relationship between XBP1 expres-sion and sugar metabolism, the influence of XBP1 repression on the survival rate of glioma cells under normoxia and hypoxia, and the influence of XBP1 on glioma cell glycolysis. Methods:We tested XBP1 activation in human glioma cell lines cultured under normoxia and hypoxia. XBP1 expression was repressed with siRNA technology. Cells were treated with oxidative phosphorylation inhibitor. We then detected the variation in cell apoptosis, sugar metabolism mode, and cell apoptosis and glycolysis products under normoxia and hypoxia. Results:XBP1 activation increased under hypoxia. Silencing XBP1 expression reduced glioma cell survival level, ATP and lactic acid production, and glucose consumption under hypoxia. After inhibiting cell oxidative phosphorylation, XBP1 repression significantly reduced the survival level of glioma cells. Conclusion:Hypoxia can activate XBP1 in glioma cells. Under hypoxia, XBP1 silencing de-presses cell activity and glycolysis. Glycolysis of glioma cells under hypoxia depends on XBP1 activation.
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