MYC and metabolism on the path to cancer

被引：258
|
作者：
Hsieh, Annie L. [1 ,2 ,3 ]
Walton, Zandra E. [1 ,2 ]
Altman, Brian J. [1 ,2 ]
Stine, Zachary E. [1 ,2 ]
Dang, Chi V. [1 ,2 ,4 ]
机构：
[1] Univ Penn, Abramson Family Canc Res Inst, Perelman Sch Med, Philadelphia, PA 19104 USA
[2] Univ Penn, Abramson Canc Ctr, Perelman Sch Med, Philadelphia, PA 19104 USA
[3] Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21205 USA
[4] Univ Penn, Dept Med, Div Hematol Oncol, Perelman Sch Med, Philadelphia, PA 19104 USA
来源：
SEMINARS IN CELL & DEVELOPMENTAL BIOLOGY | 2015年 / 43卷
基金：
美国国家卫生研究院;
关键词：
Myc; Metabolism; Cancer; mTOR; INITIATION-FACTOR; 4E; FATTY-ACID SYNTHESIS; C-MYC; GLUTAMINE-METABOLISM; TRANSLATION INITIATION; TRANSCRIPTION FACTOR; PROTEIN-SYNTHESIS; BURKITT-LYMPHOMA; DROSOPHILA-MYC; UP-REGULATION;
D O I：
10.1016/j.semcdb.2015.08.003
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
The MYC proto-oncogene is frequently deregulated in human cancers, activating genetic programs that orchestrate biological processes to promote growth and proliferation. Altered metabolism characterized by heightened nutrients uptake, enhanced glycolysis and glutaminolysis and elevated fatty acid and nucleotide synthesis is the hallmark of MYC-driven cancer. Recent evidence strongly suggests that Mycdependent metabolic reprogramming is critical for tumorigenesis, which could be attenuated by targeting specific metabolic pathways using small drug-like molecules. Understanding the complexity of MYCmediated metabolic re-wiring in cancers as well as how MYC cooperates with other metabolic drivers such as mammalian target of rapamycin (mTOR) will provide translational opportunities for cancer therapy. (C) 2015 Published by Elsevier Ltd.
引用
收藏
页码：11 / 21
页数：11
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