MYC on the Path to Cancer

被引：2667

作者：

Dang, Chi V. ^{[1
]}

机构：

[1] Univ Penn, Perelman Sch Med, Abramson Canc Ctr,Div Hematol Oncol, Abramson Family Canc Res Inst,Dept Med, Philadelphia, PA 19104 USA

来源：

CELL | 2012年 / 149卷 / 01期

基金：

美国国家卫生研究院;

关键词：

ONCOGENE-INDUCED SENESCENCE; ENDOTHELIAL GROWTH-FACTOR; LONG-RANGE INTERACTION; C-MYC; N-MYC; IN-VIVO; TRANSCRIPTIONAL ACTIVATION; BURKITT-LYMPHOMA; GENE-EXPRESSION; DROSOPHILA-MYC;

D O I：

10.1016/j.cell.2012.03.003

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：

The MYC oncogene contributes to the genesis of many human cancers. Recent insights into its expression and function have led to therapeutic opportunities. MYC's activation by bromodomain proteins could be inhibited by drug-like molecules, resulting in tumor inhibition in vivo. Tumor growth can also be curbed by pharmacologically uncoupling bioenergetic pathways involving glucose or glutamine metabolism from Myc-induced cellular biomass accumulation. Other approaches to halt Myc on the path to cancer involve targeting Myc-Max dimerization or Myc-induced microRNA expression. Here the richness of our understanding of MYC is reviewed, highlighting new biological insights and opportunities for cancer therapies.

引用

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页码：22 / 35

页数：14

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