细胞生长
PI3K/AKT/mTOR通路
生物
细胞生物学
信号转导
细胞周期
蛋白激酶B
厌氧糖酵解
谷氨酰胺
瓦博格效应
癌细胞
营养感应
重编程
糖酵解
癌症研究
癌症
细胞
代谢途径
谷氨酰胺分解
肿瘤微环境
碳水化合物代谢
细胞代谢
癌变
干细胞
生物化学
新陈代谢
基因
遗传学
氨基酸
作者
Ralph J. DeBerardinis,Julian J. Lum,Georgia Hatzivassiliou,Craig B. Thompson
标识
DOI:10.1016/j.cmet.2007.10.002
摘要
Cell proliferation requires nutrients, energy, and biosynthetic activity to duplicate all macromolecular components during each passage through the cell cycle. It is therefore not surprising that metabolic activities in proliferating cells are fundamentally different from those in nonproliferating cells. This review examines the idea that several core fluxes, including aerobic glycolysis, de novo lipid biosynthesis, and glutamine-dependent anaplerosis, form a stereotyped platform supporting proliferation of diverse cell types. We also consider regulation of these fluxes by cellular mediators of signal transduction and gene expression, including the phosphatidylinositol 3-kinase (PI3K)/Akt/mTOR system, hypoxia-inducible factor 1 (HIF-1), and Myc, during physiologic cell proliferation and tumorigenesis.
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