Márquez Javier, Alonso Francisco J, Matés José M, Segura Juan A, Martín-Rufián Mercedes, Campos-Sandoval José A
Canceromics lab, Departamento de Biología Molecular y Bioquímica, Facultad de Ciencias, Instituto de Biomedicina de Málaga (IBIMA), Universidad de Málaga, 29071, Málaga, Spain.
Neurochem Res. 2017 Jun;42(6):1735-1746. doi: 10.1007/s11064-017-2212-1. Epub 2017 Mar 9.
Cancer cells develop and succeed by shifting to different metabolic programs compared with their normal cell counterparts. One of the classical hallmarks of cancer cells is their higher glycolysis rate and lactate production even in the presence of abundant O (Warburg effect). Another common metabolic feature of cancer cells is a high rate of glutamine (Gln) consumption normally exceeding their biosynthetic and energetic needs. The term Gln addiction is now widely used to reflect the strong dependence shown by most cancer cells for this essential nitrogen substrate after metabolic reprogramming. A Gln/glutamate (Glu) cycle occurs between host tissues and the tumor in order to maximize its growth and proliferation rates. The mechanistic basis for this deregulated tumor metabolism and how these changes are connected to oncogenic and tumor suppressor pathways are becoming increasingly understood. Based on these advances, new avenues of research have been initiated to find novel therapeutic targets and to explore strategies that interfere with glutamine metabolism as anticancer therapies. In this review, we provided an updated overview of glutamine addiction in glioma, the most prevalent type of brain tumor.
与正常细胞相比,癌细胞通过转向不同的代谢程序来发展并得以生存。癌细胞的一个经典特征是即使在有充足氧气的情况下,其糖酵解速率和乳酸生成也较高(瓦伯格效应)。癌细胞的另一个常见代谢特征是谷氨酰胺(Gln)消耗率很高,通常超过其生物合成和能量需求。“谷氨酰胺成瘾”一词现在被广泛用于反映大多数癌细胞在代谢重编程后对这种必需氮底物的强烈依赖。宿主组织和肿瘤之间会发生谷氨酰胺/谷氨酸(Glu)循环,以最大化其生长和增殖速率。这种失调的肿瘤代谢的机制基础以及这些变化如何与致癌和肿瘤抑制途径相关联,人们的了解越来越多。基于这些进展,已经开启了新的研究途径,以寻找新的治疗靶点,并探索干扰谷氨酰胺代谢作为抗癌疗法的策略。在这篇综述中,我们提供了关于胶质瘤(最常见的脑瘤类型)中谷氨酰胺成瘾的最新概述。