Cancer Cell Metabolism: One Hallmark, Many Faces

被引:738
作者
Cantor, Jason R. [1 ,2 ]
Sabatini, David M. [1 ,2 ,3 ,4 ,5 ]
机构
[1] Whitehead Inst Biomed Res, Cambridge, MA 02142 USA
[2] Broad Inst Harvard & Massachusetts Inst Technol, Cambridge, MA USA
[3] Koch Inst Integrat Canc Res, Cambridge, MA USA
[4] MIT, Howard Hughes Med Inst, Cambridge, MA USA
[5] MIT, Dept Biol, Cambridge, MA USA
关键词
PYRUVATE-KINASE M2; ACUTE LYMPHOBLASTIC-LEUKEMIA; L-ASPARAGINASE RESISTANCE; GLUTAMINE-METABOLISM; FATTY-ACID; C-MYC; TUMOR MICROENVIRONMENT; ALPHA-KETOGLUTARATE; GLUCOSE-METABOLISM; AEROBIC GLYCOLYSIS;
D O I
10.1158/2159-8290.CD-12-0345
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Cancer cells must rewire cellular metabolism to satisfy the demands of growth and proliferation. Although many of the metabolic alterations are largely similar to those in normal proliferating cells, they are aberrantly driven in cancer by a combination of genetic lesions and nongenetic factors such as the tumor microenvironment. However, a single model of altered tumor metabolism does not describe the sum of metabolic changes that can support cell growth. Instead, the diversity of such changes within the metabolic program of a cancer cell can dictate by what means proliferative rewiring is driven, and can also impart heterogeneity in the metabolic dependencies of the cell. A better understanding of this heterogeneity may enable the development and optimization of therapeutic strategies that target tumor metabolism.
引用
收藏
页码:881 / 898
页数:18
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