Metabolic reprogramming and cancer progression

被引:1180
|
作者
Faubert, Brandon [1 ]
Solmonson, Ashley [1 ]
DeBerardinis, Ralph J. [1 ,2 ]
机构
[1] Univ Texas Southwestern Med Ctr Dallas, Childrens Med Ctr, Res Inst, 5323 Harry Hines Blvd, Dallas, TX 75390 USA
[2] Univ Texas Southwestern Med Ctr Dallas, Howard Hughes Med Inst, 5323 Harry Hines Blvd, Dallas, TX 75390 USA
基金
加拿大健康研究院;
关键词
CIRCULATING TUMOR-CELLS; BREAST-CANCER; LUNG-CANCER; GLIOBLASTOMA-MULTIFORME; SUCCINATE-DEHYDROGENASE; OXIDATIVE STRESS; METASTASIS; MUTATIONS; HETEROGENEITY; LKB1;
D O I
10.1126/science.aaw5473
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Metabolic reprogramming is a hallmark of malignancy. As our understanding of the complexity of tumor biology increases, so does our appreciation of the complexity of tumor metabolism. Metabolic heterogeneity among human tumors poses a challenge to developing therapies that exploit metabolic vulnerabilities. Recent work also demonstrates that the metabolic properties and preferences of a tumor change during cancer progression. This produces distinct sets of vulnerabilities between primary tumors and metastatic cancer, even in the same patient or experimental model. We review emerging concepts about metabolic reprogramming in cancer, with particular attention on why metabolic properties evolve during cancer progression and how this information might be used to develop better therapeutic strategies.
引用
收藏
页码:152 / +
页数:11
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