Therapeutic targets in cancer cell metabolism and autophagy

被引:275
作者
Cheong, Heesun [1 ]
Lu, Chao [1 ,2 ]
Lindsten, Tullia [3 ]
Thompson, Craig B. [1 ]
机构
[1] Mem Sloan Kettering Canc Ctr, Sloan Kettering Inst, Canc Biol & Genet Program, New York, NY 10021 USA
[2] Univ Penn, Perelman Sch Med, Dept Canc Biol, Philadelphia, PA 19104 USA
[3] Mem Sloan Kettering Canc Ctr, Program Immunol, Sloan Kettering Inst, New York, NY 10021 USA
基金
美国国家卫生研究院;
关键词
HISTONE DEACETYLASE INHIBITOR; MALIGNANT GLIOMA-CELLS; PYRUVATE-KINASE M2; ISOLATED RAT HEPATOCYTES; BREAST-CANCER; GLUTAMINE-METABOLISM; TUMOR PROGRESSION; MAMMARY TUMORIGENESIS; INDUCED APOPTOSIS; ARSENIC TRIOXIDE;
D O I
10.1038/nbt.2285
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
The metabolism of cancer cells is reprogrammed both by oncogene signaling and by dysregulation of metabolic enzymes. The resulting altered metabolism supports cellular proliferation and survival but leaves cancer cells dependent on a continuous supply of nutrients. Thus, many metabolic enzymes have become targets for new cancer therapies. Recently, two processes-expression of specific isoforms of metabolic enzymes and autophagy-have been shown to be crucial for the adaptation of tumor cells to changes in nutrient availability. An increasing number of approved and experimental therapeutics target these two processes. A better understanding of the molecular basis of cancer-associated metabolic changes may lead to improved cancer therapies.
引用
收藏
页码:671 / 678
页数:8
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