氧化磷酸化
巴基斯坦卢比
厌氧糖酵解
MFN2型
糖酵解
线粒体融合
细胞生物学
生物
瓦博格效应
线粒体
丙酮酸激酶
生物化学
新陈代谢
线粒体DNA
基因
作者
Tong Li,Jin Han,Liangjie Jia,Xiao Hu,Liqun Chen,Yiguo Wang
出处
期刊:Protein & Cell
[Springer Nature]
日期:2019-03-18
卷期号:10 (8): 583-594
被引量:101
标识
DOI:10.1007/s13238-019-0618-z
摘要
A change in the metabolic flux of glucose from mitochondrial oxidative phosphorylation (OXPHOS) to aerobic glycolysis is regarded as one hallmark of cancer. However, the mechanisms underlying the metabolic switch between aerobic glycolysis and OXPHOS are unclear. Here we show that the M2 isoform of pyruvate kinase (PKM2), one of the rate-limiting enzymes in glycolysis, interacts with mitofusin 2 (MFN2), a key regulator of mitochondrial fusion, to promote mitochondrial fusion and OXPHOS, and attenuate glycolysis. mTOR increases the PKM2:MFN2 interaction by phosphorylating MFN2 and thereby modulates the effect of PKM2:MFN2 on glycolysis, mitochondrial fusion and OXPHOS. Thus, an mTOR-MFN2-PKM2 signaling axis couples glycolysis and OXPHOS to modulate cancer cell growth.
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