Akt-dependent transformation: there is more to growth than just surviving

被引:334
作者
Plas, DR
Thompson, CB
机构
[1] Univ Cincinnati, Dept Genome Sci, Genome Res Inst, Cincinnati, OH 45237 USA
[2] Univ Penn, Abramson Canc Res Inst, Dept Canc Biol, Philadelphia, PA 19146 USA
关键词
glycolysis; metabolism; forkhead; FOXO; TSC2; feedback;
D O I
10.1038/sj.onc.1209097
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Activation of the Akt/PKB protein kinase family triggers increases in cell size, metabolism and survival. Akt coordinately regulates these fundamental cellular processes through phosphorylation-dependent inactivation of tumor suppressors and activation of trophic signaling. Akt signaling stimulates transport and metabolism of both glucose and amino acids, which in turn support mTOR-dependent increases in protein translation. In addition, Akt activation directs cells to undertake a metabolic conversion from oxidative phosphorylation to aerobic glycolysis. Although this conversion promotes cell growth, it also renders cell survival dependent on a continuous supply of extracellular nutrients, which themselves are required regulatory elements in Akt signal transduction.
引用
收藏
页码:7435 / 7442
页数:8
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