Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate

被引:2516
作者
Ward, Patrick S. [1 ,2 ]
Thompson, Craig B. [1 ]
机构
[1] Mem Sloan Kettering Canc Ctr, Canc Biol & Genet Program, New York, NY 10065 USA
[2] Univ Penn, Perelman Sch Med, Cell & Mol Biol Grad Grp, Philadelphia, PA 19104 USA
关键词
PYRUVATE-KINASE M2; ATP-CITRATE LYASE; GLUTAMINE-METABOLISM; AEROBIC GLYCOLYSIS; IDH2; MUTATIONS; ALPHA-KETOGLUTARATE; TUMOR-CELLS; ONCOMETABOLITE; 2-HYDROXYGLUTARATE; NUCLEAR TRANSLOCATION; TRANSFORMED-CELLS;
D O I
10.1016/j.ccr.2012.02.014
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Cancer metabolism has long been equated with aerobic glycolysis, seen by early biochemists as primitive and inefficient. Despite these early beliefs, the metabolic signatures of cancer cells are not passive responses to damaged mitochondria but result from oncogene-directed metabolic reprogramming required to support anabolic growth. Recent evidence suggests that metabolites themselves can be oncogenic by altering cell signaling and blocking cellular differentiation. No longer can cancer-associated alterations in metabolism be viewed as an indirect response to cell proliferation and survival signals. We contend that altered metabolism has attained the status of a core hallmark of cancer.
引用
收藏
页码:297 / 308
页数:12
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