在细胞亚群水平上分析能量代谢

K. Benihoud, C. Brenner
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引用次数: 0

摘要

尽管癌症是一种复杂的病理学,既有遗传病因,也有非遗传病因,但其特征是一系列有限的特征,包括能量代谢重编程[1]。很久以前,O.Warburg发现肿瘤代谢偏向于糖酵解,即所谓的Warburg效应。事实上,肿瘤细胞表现出葡萄糖摄取增加和葡萄糖发酵为乳酸[2]。自从这些开创性的工作以来,报道了肿瘤代谢的不同变化,如谷氨酰胺的摄取失调或营养获取的新模式[3]。一般来说,由于组成性合成代谢和分解代谢激活,癌症细胞表现出高增殖率。此外,通过在肿瘤微环境(TME)中竞争营养、诱导缺氧和释放抑制分子,肿瘤显著影响免疫细胞代谢[4]。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Profiling the Energy Metabolism at the Cell Subpopulation Level
Although being a complex pathology with genetic as well as non-genetic etiologies, cancer is characterized by a limited series of hallmarks including energetic metabolism reprogramming [1]. Long ago O. Warburg unraveled a bias of tumor metabolism in favor of glycolysis, the socalled Warburg effect. Indeed, tumor cells display both an increase in glucose uptake and fermentation of glucose to lactate [2]. Since these pioneering works, different alterations of tumor metabolism were reported such as deregulated uptake of glutamine or new modes of nutrient acquisition [3]. In general, cancer cells exhibit a high rate of proliferation due to constitutive anabolism and catabolism activation. Moreover, by competing for nutrients, inducing hypoxia and releasing inhibitory molecules in tumor microenvironment (TME), tumors dramatically affect immune cell metabolism [4].
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