MYC and metabolism on the path to cancer.
MYC and metabolism on the path to cancer.
复制标题
DOI：
10.1016/j.semcdb.2015.08.003
复制
发表时间：
2015-07
影响因子：
7.3
通讯作者：
Dang CV
中科院分区：
文献类型：
--
作者：
Hsieh AL;Walton ZE;Altman BJ;Stine ZE;Dang CV
MYC原癌基因在人类癌症中经常被解除调控，激活协调生物过程以促进生长和增殖的遗传程序。代谢改变的特征是营养摄取增加，糖酵解和谷氨酰胺溶解增强，脂肪酸和核苷酸合成升高，这是myc驱动的癌症的标志。最近的证据强烈表明，myc依赖性代谢重编程对肿瘤发生至关重要，可以通过使用小药物样分子靶向特定的代谢途径来减弱。了解癌症中MYC介导的代谢重新布线的复杂性，以及MYC如何与其他代谢驱动因素（如哺乳动物雷帕霉素靶点（mTOR））合作，将为癌症治疗提供转化机会。
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 Myc-dependent metabolic reprogramming is critical for tumorigenesis, which could be attenuated by targeting specific metabolic pathways using small drug-like molecules. Understanding the complexity of MYC-mediated 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.