Department of Pharmacology and Cancer Biology, Department of Immunology, Sarah W, Stedman Nutrition and Metabolism Center, Duke University, Durham, NC, 27710, USA.
Cancer Metab. 2013 Jan 23;1(1):5. doi: 10.1186/2049-3002-1-5.
Metabolic reprogramming is a key event in tumorigenesis to support cell growth, and cancer cells frequently become both highly glycolytic and glutamine dependent. Similarly, T lymphocytes (T cells) modify their metabolism after activation by foreign antigens to shift from an energetically efficient oxidative metabolism to a highly glycolytic and glutamine-dependent metabolic program. This metabolic transition enables T cell growth, proliferation, and differentiation. In both activated T cells and cancer cells metabolic reprogramming is achieved by similar mechanisms and offers similar survival and cell growth advantages. Activated T cells thus present a useful model with which to study the development of tumor metabolism. Here, we review the metabolic similarities and distinctions between activated T cells and cancer cells, and discuss both the common signaling pathways and master metabolic regulators that lead to metabolic rewiring. Ultimately, understanding how and why T cells adopt a cancer cell-like metabolic profile may identify new therapeutic strategies to selectively target tumor metabolism or inflammatory immune responses.
代谢重编程是肿瘤发生的关键事件，以支持细胞生长，癌细胞经常变得高度糖酵解和谷氨酰胺依赖。同样，T 淋巴细胞（T 细胞）在被外来抗原激活后改变其代谢，从能量有效的氧化代谢转变为高度糖酵解和谷氨酰胺依赖的代谢程序。这种代谢转变使 T 细胞能够生长、增殖和分化。在激活的 T 细胞和癌细胞中，代谢重编程是通过类似的机制实现的，并提供了类似的生存和细胞生长优势。因此，激活的 T 细胞为研究肿瘤代谢的发展提供了一个有用的模型。在这里，我们综述了激活的 T 细胞和癌细胞之间的代谢相似性和差异，并讨论了导致代谢重排的共同信号通路和主要代谢调节因子。最终，了解 T 细胞如何以及为什么采用类似于癌细胞的代谢特征，可能会确定新的治疗策略，以选择性地靶向肿瘤代谢或炎症免疫反应。
