Tumour friend or foe

摘要

Tumour cells face various metabolic stresses as they arise and progress. Early-stage tumours that have not yet recruited new blood vessels to supply them with nutrients will be short of both glucose and oxygen1, and some cells face metabolic stress when they make the transition from a normal to a cancerous state and become detached from the extracellular matrix, their normal environment. Additionally, some mutations that trigger tumour formation accelerate certain cellular metabolic programs and thereby cause stress. A protein called AMP-activated protein kinase (AMPK) is a central sensor of cellular metabolism. It is activated during situations of metabolic stress that lower the intracellu-lar levels of ATP, a crucial energy-supplying molecule. On page 661 of this issue, Jeon et al. report a mechanism by which AMPK dictates tumour-cell survival, and the surprising implication that it may have a cancer-promoting role in some contexts.