Balancing biosynthesis and bioenergetics: metabolic programs in oncogenesis

被引：53

作者：

Barger, Jennifer F. ^{[1
]}

Plas, David R. ^{[1
]}

机构：

[1] Univ Cincinnati, Dept Canc & Cell Biol, Cincinnati, OH 45267 USA

来源：

关键词：

FATTY-ACID SYNTHASE; ACTIVATED PROTEIN-KINASE; ATP-CITRATE LYASE; ACETYL-COA CARBOXYLASE; CONGESTIVE-HEART-FAILURE; HYPOXIA-INDUCIBLE FACTOR; TRACT-BINDING PROTEIN; RENAL-CELL CARCINOMA; BREAST-CANCER CELLS; C-MYC;

D O I：

10.1677/ERC-10-0106

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Cancer biologists' search for new chemotherapy targets is reinvigorating the study of how cancer cell metabolism determines both oncogenic potential and chemotherapeutic responses. Oncogenic metabolic programs support the bioenergetics associated with resistance to programed cell death and provide biosynthetic building blocks for cell growth and mitogenesis. Both signal transduction pathway activation and direct mutations in key metabolic enzymes can activate the metabolic programs that support cancer cell growth. Cancer-associated metabolic programs include glycolysis, glutamine oxidation, and fatty acid metabolism. Recent observations are revealing the regulatory mechanisms that activate cancer-associated metabolism, and the competitive advantages provided to transformed cells by their metabolic programs. In this study, we review recent results illustrating the mechanisms and functional impact of each of these oncogenic metabolic programs in cancer cell growth and survival. Endocrine-Related Cancer (2010) 17 R287-R304

引用

页码：R287 / R304

页数：18

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