Glucose metabolism has been suggested to be an integral component of the metabolic detoxification pathways, which protect tumor cells from H2O2
The results of the current studies showed that treatment of human breast cancer cells with 2-deoxy-D-glucose causes metabolic oxidative stress that is accompanied by increases in steadystate levels of glutamate cysteine ligasemRNA, GCL activity, and glutathione content
A similar analysis of the RNA levels of the modifier subunit of the GCL enzyme showed no significant increases at the 8- or 24-hour time points of 2-deoxy-D-glucose exposure. These results show that treatment of human breast cancer cells with 2-deoxy-D-glucose induced the increased expression of GCLC as well as GCL activity
These results provide further support for the hypothesis that GCL is a protective enzyme up-regulated in response to metabolic oxidative stress induced by exposure of human cancer cells to 2-deoxy-D-glucose
Cancer cells metabolize more glucose than their normal cell counterparts, and this metabolic characteristic is exploited in positron emission tomography imaging to localize cancerous tissue using F18-2-deoxy-D-glucose
2-deoxy-D-glucose caused a significant increase in the GCL activity that was accompanied by increased steady-state levels of mRNA coding for GCLC. These data are consistent with the hypothesis that MDA-MB231 human breast cancer cells induce an adaptive response to treatment with 2-deoxy-D-glucose that involves the up-regulation of GSH synthesis via increased GCL activity, resulting in enhanced 2-deoxy-D-glucose resistance
These data are consistent with the hypothesis that MDA-MB231 human breast cancer cells induce an adaptive response to treatment with 2-deoxy-D-glucose that involves the up-regulation of GSH synthesis via increased glutamate cysteine ligase activity, resulting in enhanced 2-deoxy-D-glucose resistance
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