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首页> 外文期刊>Cancer biology & therapy >The radiosensitization effect of 2-deoxy-D-glucose on human glioma cells.
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The radiosensitization effect of 2-deoxy-D-glucose on human glioma cells.

机译:2-脱氧-D-葡萄糖对人神经胶质瘤细胞的放射增敏作用。

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摘要

2-deoxygIucose (2-DG), a glucose analogue, blocks glycolysis, inhibits ATP generation interferes with protein glycosylation, histone regulation, and has been tested in rnultinU preclinical studies as a potential anticancer. Few studies found that 2-DG, lowers intra cellular ATP levels significantly below 15%, and, as a consequence, effect cell death Several cell culture studies have highlighted the higher rates of glucose utilization and lactate production in tumor cells5'6 and thus, it is not surprising that, in cancer models glucose deprivation is known to cause cytotoxicity in vitro and in vivo by activating multiple signal transduction pathways that are associated with angiogenesis and expression of cellular oncogenes. Evidences suggest that 2-DG causes oxidative stress-mediated cell death in tumor cells by creating a glucose deprivation effect. Both in vitro and in vivo tumor models suggest that 2-DG enhances radiosensitization effect; however, the exact mechanism of the radiosensitization of 2-DGis not fully established.
机译:2-deoxygIucose(2-DG),一种葡萄糖类似物,可阻止糖酵解,抑制ATP的生成,干扰蛋白质糖基化,组蛋白调节,并已在rnultinU临床前研究中作为潜在的抗癌药物进行了测试。很少有研究发现2-DG可将细胞内A​​TP的水平显着降低至15%以下,并因此影响细胞死亡。几项细胞培养研究突显了肿瘤细胞中较高的葡萄糖利用率和乳酸生成率5'6,因此,不足为奇的是,在癌症模型中,已知葡萄糖剥夺通过激活与血管生成和细胞癌基因表达相关的多种信号转导途径,在体外和体内引起细胞毒性。有证据表明2-DG通过产生葡萄糖剥夺效应而在肿瘤细胞中引起氧化应激介导的细胞死亡。体外和体内肿瘤模型均表明2-DG可增强放射增敏作用。但是,2-DG放射增敏的确切机制尚未完全建立。

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