Exploiting the bad eating habits of Ras-driven cancers.

Exploiting the bad eating habits of Ras-driven cancers.
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DOI:
10.1101/gad.228122.113
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发表时间:
2013-10-01
影响因子:
10.5
通讯作者:
White E
White E
中科院分区:
生物学1区
文献类型:
--
作者:
White E

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致癌Ras产生生长的构建模块,为代谢途径提供燃料,并支持新陈代谢。在这篇综述中,白色讨论的进展,揭示了新的机会,削弱了关键的代谢效应器功能的Ras。致癌Ras促进葡萄糖发酵和谷氨酰胺的使用,以提供中央碳代谢,但如何以及为什么最近才出现。Ras介导的代谢重编程产生生长的构建模块并促进抗氧化防御。为了给代谢途径提供燃料,Ras清除细胞外蛋白质和脂质。为了促进新陈代谢和减轻压力,Ras通过自噬激活细胞的自我吞噬和蛋白质和细胞器的再循环。靶向Ras驱动的癌症的这些独特特征提供了癌症治疗的新方法。
Oncogenic Ras generates building blocks for growth, fuels metabolic pathways, and bolsters metabolism. In this review, White discusses advances that shed light on new opportunities with which to cripple the critical metabolic effector functions of Ras. Oncogenic Ras promotes glucose fermentation and glutamine use to supply central carbon metabolism, but how and why have only emerged recently. Ras-mediated metabolic reprogramming generates building blocks for growth and promotes antioxidant defense. To fuel metabolic pathways, Ras scavenges extracellular proteins and lipids. To bolster metabolism and mitigate stress, Ras activates cellular self-cannibalization and recycling of proteins and organelles by autophagy. Targeting these distinct features of Ras-driven cancers provides novel approaches to cancer therapy.
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