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首页> 外文期刊>Cell metabolism >AMPK is a negative regulator of the warburg effect and suppresses tumor growth in vivo
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AMPK is a negative regulator of the warburg effect and suppresses tumor growth in vivo

机译：AMPK是Warburg效应的负调节剂，可抑制体内肿瘤生长

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摘要

AMPK is a metabolic sensor that helps maintain cellular energy homeostasis. Despite evidence linking AMPK with tumor suppressor functions, the role of AMPK in tumorigenesis and tumor metabolism is unknown. Here we show that AMPK negatively regulates aerobic glycolysis (the Warburg effect) in cancer cells and suppresses tumor growth in vivo. Genetic ablation of the α1 catalytic subunit of AMPK accelerates Myc-induced lymphomagenesis. Inactivation of AMPKα in both transformed and nontransformed cells promotes a metabolic shift to aerobic glycolysis, increased allocation of glucose carbon into lipids, and biomass accumulation. These metabolic effects require normoxic stabilization of the hypoxia-inducible factor-1α (HIF-1α), as silencing HIF-1α reverses the shift to aerobic glycolysis and the biosynthetic and proliferative advantages conferred by reduced AMPKα signaling. Together our findings suggest that AMPK activity opposes tumor development and that its loss fosters tumor progression in part by regulating cellular metabolic pathways that support cell growth and proliferation.
机译：AMPK是一种代谢传感器，可帮助维持细胞能量稳态。尽管有证据表明AMPK与肿瘤抑制功能有关，但AMPK在肿瘤发生和肿瘤代谢中的作用尚不清楚。在这里，我们显示AMPK在癌细胞中负调节有氧糖酵解作用（Warburg效应），并抑制体内肿瘤的生长。 AMPK的α1催化亚基的遗传消融加速了Myc诱导的淋巴瘤的形成。转化细胞和未转化细胞中AMPKα的失活均促进了向有氧糖酵解的代谢转变，增加了葡萄糖碳在脂质中的分配以及生物量的积累。这些代谢作用需要低氧诱导因子1α（HIF-1α）的常氧稳定，因为沉默HIF-1α可逆向有氧糖酵解的转变，并通过减少AMPKα信号传导提供生物合成和增殖优势。我们的研究结果共同表明，AMPK活性可对抗肿瘤的发展，其丧失部分通过调节支持细胞生长和增殖的细胞代谢途径来促进肿瘤的进展。

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