Camarda Roman, Williams Jeremy, Goga Andrei
Department of Cell and Tissue Biology, University of California, San FranciscoSan Francisco, CA, USA.
Biomedical Sciences Graduate Program, University of California, San FranciscoSan Francisco, CA, USA.
Front Cell Dev Biol. 2017 Apr 11;5:35. doi: 10.3389/fcell.2017.00035. eCollection 2017.
The past few decades have welcomed tremendous advancements toward understanding the functional significance of altered metabolism during tumorigenesis. However, many conclusions drawn from studies of cancer cells in a dish (i.e., ) have been put into question as multiple lines of evidence have demonstrated that the metabolism of cells can differ significantly from that of primary tumors (. This realization, along with the need to identify tissue-specific vulnerabilities of driver oncogenes, has led to an increased focus on oncogene-dependent metabolic programming . The oncogene c-MYC (MYC) is overexpressed in a wide variety of human cancers, and while its ability to alter cellular metabolism is well-established, translating the metabolic requirements, and vulnerabilities of MYC-driven cancers to the clinic has been hindered by disparate findings from and models. This review will provide an overview of the strategies, mechanisms, and conclusions generated thus far by studying MYC's regulation of metabolism in various cancer models.
在过去几十年里，我们在理解肿瘤发生过程中代谢改变的功能意义方面取得了巨大进展。然而，许多基于培养皿中癌细胞研究得出的结论（即 ）受到了质疑，因为多条证据表明，细胞代谢可能与原发性肿瘤的代谢存在显著差异（ ）。这一认识，以及识别驱动癌基因组织特异性脆弱性的需求，导致人们越来越关注癌基因依赖性代谢编程（ ）。癌基因c-MYC（MYC）在多种人类癌症中过度表达，虽然其改变细胞代谢的能力已得到充分证实，但将MYC驱动癌症的代谢需求和脆弱性转化到临床实践中却受到 模型和 模型不同研究结果的阻碍。本综述将概述迄今为止通过研究MYC在各种癌症模型中对代谢的调控所产生的 策略、机制和结论。
