自噬
生物
癌变
下调和上调
癌症研究
糖酵解
代谢途径
信号转导
癌症
谷氨酰胺
表型
细胞生物学
新陈代谢
生物化学
遗传学
基因
细胞凋亡
氨基酸
作者
Jonathan M. DeLiberty,Ryan Robb,Claire E. Gates,Kirsten L. Bryant
出处
期刊:Elsevier eBooks
[Elsevier]
日期:2022-01-01
卷期号:: 267-304
被引量:1
标识
DOI:10.1016/bs.acr.2021.07.010
摘要
RAS mutations are among the most frequent oncogenic drivers observed in human cancers. With a lack of available treatment options, RAS-mutant cancers account for many of the deadliest cancers in the United States. Recent studies established that altered metabolic requirements are a hallmark of cancer, and many of these alterations are driven by aberrant RAS signaling. Specifically, RAS-driven cancers are characterized by upregulated glycolysis, the differential channeling of glycolytic intermediates, upregulated nutrient scavenging pathways such as autophagy and macropinocytosis, and altered glutamine utilization and mitochondrial function. This unique metabolic landscape promotes tumorigenesis, proliferation, survival in nutrient deficient environments and confers resistance to conventional cytotoxic and targeted therapies. Emerging work demonstrates how these dependencies can be therapeutically exploited in vitro and in vivo with many metabolic inhibitors currently in clinical trials. This review aims to outline the unique metabolic requirements induced by aberrant RAS signaling and how these altered dependencies present opportunities for therapeutic intervention.
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