Targeting Metabolism for Cancer Therapy

被引：726

作者：

Luengo, Alba ^{[1
,2
]}

Gui, Dan Y. ^{[1
,2
]}

Vander Heiden, Matthew G. ^{[1
,2
,3
]}

机构：

[1] MIT, Koch Inst Integrat Canc Res, 77 Massachusetts Ave, Cambridge, MA 02139 USA

[2] MIT, Dept Biol, 77 Massachusetts Ave, Cambridge, MA 02139 USA

[3] Dana Farber Canc Inst, Boston, MA 02115 USA

来源：

CELL CHEMICAL BIOLOGY | 2017年 / 24卷 / 09期

关键词：

PEGYLATED ARGININE DEIMINASE; CELL LUNG-CANCER; FATTY-ACID SYNTHESIS; ATP CITRATE LYASE; ARGININOSUCCINATE SYNTHETASE EXPRESSION; POSITRON-EMISSION-TOMOGRAPHY; NOVO PYRIMIDINE SYNTHESIS; ELECTRON-TRANSPORT CHAIN; SMALL-MOLECULE INHIBITOR; MITOCHONDRIAL COMPLEX I;

D O I：

10.1016/j.chembiol.2017.08.028

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Metabolic reprogramming contributes to tumor development and introduces metabolic liabilities that can be exploited to treat cancer. Chemotherapies targeting metabolism have been effective cancer treatments for decades, and the success of these therapies demonstrates that a therapeutic window exists to target malignant metabolism. New insights into the differential metabolic dependencies of tumors have provided novel therapeutic strategies to exploit altered metabolism, some of which are being evaluated in preclinical models or clinical trials. Here, we review our current understanding of cancer metabolism and discuss how this might guide treatments targeting the metabolic requirements of tumor cells.

引用

页码：1161 / 1180

页数：20

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