Sebastian Carlos
Massachusetts General Hospital Cancer Center, Harvard Medical School, Cambridge Street, Simches Building, 4th floor, Boston, MA 02114.
Crit Rev Oncog. 2014;19(5):363-82. doi: 10.1615/critrevoncog.2014011844.
Metabolic reprogramming has recently emerged as a fundamental trait of cancer cells. Initially thought to be a consequence of rapid cell proliferation, recent data have reset this idea by demonstrating that metabolic reprogramming can actually drive tumorigenesis. The cancer stem cell (CSC) theory predicts that only a small subpopulation of cancer cells with stem cell properties, which derive from the cancer cell of origin, possesses tumor-initiating potential. However, whether metabolic reprogramming drives tumor formation by regulating the genesis of CSCs is not known. Importantly, the metabolic properties of stem cells and cancer cells are strikingly similar, and metabolic reprogramming is a key factor controlling stemness in these cells. This article reviews the current understanding of cancer metabolism and how it mirrors the metabolic requirements of stem cells. These two concepts are integrated and data demonstrating that metabolic reprogramming regulates CSCs function are discussed, suggesting that metabolic regulation of stemness could be at the origin of cancer.
代谢重编程最近已成为癌细胞的一个基本特征。最初认为这是细胞快速增殖的结果，但最近的数据通过证明代谢重编程实际上可以驱动肿瘤发生，颠覆了这一观点。癌症干细胞（CSC）理论预测，只有一小部分具有干细胞特性的癌细胞亚群（源自肿瘤起源细胞）具有肿瘤起始潜能。然而，代谢重编程是否通过调节癌症干细胞的产生来驱动肿瘤形成尚不清楚。重要的是，干细胞和癌细胞的代谢特性惊人地相似，代谢重编程是控制这些细胞干性的关键因素。本文综述了目前对癌症代谢的理解以及它如何反映干细胞的代谢需求。将这两个概念整合起来，并讨论了表明代谢重编程调节癌症干细胞功能的数据，提示干性的代谢调节可能是癌症的起源。
