文章：

PI3K-AKT网络在致癌信号传导和肿瘤代谢的接口

The PI3K–AKT network at the interface of oncogenic signalling and cancer metabolism

原文发布日期：2019-11-04

DOI: 10.1038/s41568-019-0216-7

类型: Review Article

开放获取: 否

英文摘要：

The altered metabolic programme of cancer cells facilitates their cell-autonomous proliferation and survival. In normal cells, signal transduction pathways control core cellular functions, including metabolism, to couple the signals from exogenous growth factors, cytokines or hormones to adaptive changes in cell physiology. The ubiquitous, growth factor-regulated phosphoinositide 3-kinase (PI3K)–AKT signalling network has diverse downstream effects on cellular metabolism, through either direct regulation of nutrient transporters and metabolic enzymes or the control of transcription factors that regulate the expression of key components of metabolic pathways. Aberrant activation of this signalling network is one of the most frequent events in human cancer and serves to disconnect the control of cell growth, survival and metabolism from exogenous growth stimuli. Here we discuss our current understanding of the molecular events controlling cellular metabolism downstream of PI3K and AKT and of how these events couple two major hallmarks of cancer: growth factor independence through oncogenic signalling and metabolic reprogramming to support cell survival and proliferation.

摘要翻译： 

癌细胞代谢程序的改变促进了其细胞自主性的增殖和存活。在正常细胞中，信号转导通路通过外源生长因子、细胞因子或激素信号与细胞生理适应性改变的耦合，实现对代谢等核心细胞功能的调控。普遍存在的生长因子调控型磷酸肌醇3-激酶（PI3K）-AKT信号网络通过直接调节营养转运蛋白与代谢酶，或通过调控代谢通路关键组分表达水平的转录因子，对细胞代谢产生多样化下游效应。该信号网络的异常激活是人类癌症中最常见的分子事件之一，导致细胞生长、存活及代谢调控与外源生长刺激信号解偶联。本文重点探讨目前对PI3K和AKT下游细胞代谢调控分子事件的认识，以及这些事件如何将癌症两大标志性特征——通过致癌信号实现生长因子非依赖性、通过代谢重编程支持细胞存活与增殖——相互关联的机制。

原文链接：

The PI3K–AKT network at the interface of oncogenic signalling and cancer metabolism