Targeting glucose metabolism for cancer therapy

被引:315
作者
Hamanaka, Robert B. [1 ]
Chandel, Navdeep S. [1 ,2 ,3 ]
机构
[1] Northwestern Univ, Sch Med, Dept Med, Div Pulm & Crit Care, Chicago, IL 60611 USA
[2] Northwestern Univ, Sch Med, Robert H Lurie Comprehens Canc Ctr, Chicago, IL 60611 USA
[3] Northwestern Univ, Sch Med, Dept Cell & Mol Biol, Chicago, IL 60611 USA
基金
美国国家卫生研究院;
关键词
PYRUVATE-KINASE M2; TUMOR-GROWTH; PKM2; CELLS; TRANSACTIVATION; DEHYDROGENASE; CONTRIBUTES; PROGRESSION; INHIBITION; GLYCOLYSIS;
D O I
10.1084/jem.20120162
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Cellular transformation is associated with the reprogramming of cellular pathways that control proliferation, survival, and metabolism. Among the metabolic changes exhibited by tumor cells is an increase in glucose metabolism and glucose dependence. It has been hypothesized that targeting glucose metabolism may provide a selective mechanism by which to kill cancer cells. In this minireview, we discuss the benefits that high levels of glycolysis provide for tumor cells, as well as several key enzymes required by cancer cells to maintain this high level of glucose metabolism. It is anticipated that understanding which metabolic enzymes are particularly critical for tumor cell proliferation and survival will identify novel therapeutic targets.
引用
收藏
页码:211 / 215
页数:5
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