Global Profiling Strategies for Mapping Dysregulated Metabolic Pathways in Cancer

被引：106

作者：

Benjamin, Daniel I. ^{[1
]}

Cravatt, Benjamin F. ^{[2
]}

Nomura, Daniel K. ^{[1
]}

机构：

[1] Univ Calif Berkeley, Dept Nutr Sci & Toxicol, Program Metab Biol, Berkeley, CA 94720 USA

[2] Scripps Res Inst, Dept Physiol Chem, La Jolla, CA 92037 USA

来源：

CELL METABOLISM | 2012年 / 16卷 / 05期

基金：

美国国家卫生研究院;

关键词：

FATTY-ACID SYNTHASE; PYRUVATE-KINASE M2; GLUTAMINE-METABOLISM; ALPHA-KETOGLUTARATE; AEROBIC GLYCOLYSIS; CELL-GROWTH; INHIBITOR; ISOFORM; MUTATIONS; PROMOTE;

D O I：

10.1016/j.cmet.2012.09.013

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Cancer cells possess fundamentally altered metabolism that provides a foundation to support tumorigenicity and malignancy. Our understanding of the biochemical underpinnings of cancer has benefited from the integrated utilization of large-scale profiling platforms (e.g., genomics, proteomics, and metabolomics), which, together, can provide a global assessment of how enzymes and their parent metabolic networks become altered in cancer to fuel tumor growth. This review presents several examples of how these integrated platforms have yielded fundamental insights into dysregulated metabolism in cancer. We will also discuss questions and challenges that must be addressed to more completely describe, and eventually control, the diverse metabolic pathways that support tumorigenesis.

引用

页码：565 / 577

页数：13

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