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.

中文翻译：

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PI3K-AKT网络位于致癌信号和癌症代谢的界面。

癌细胞代谢程序的改变促进了它们的细胞自主增殖和存活。在正常细胞中，信号转导通路控制着包括新陈代谢在内的核心细胞功能，以将来自外源性生长因子，细胞因子或激素的信号与细胞生理学的适应性变化相结合。普遍存在的生长因子调节的磷酸肌醇3激酶（PI3K）-AKT信号网络通过直接调节营养转运蛋白和代谢酶或控制转录因子来调节细胞关键成分的表达，从而对细胞代谢产生多种下游影响。代谢途径。该信号网络的异常激活是人类癌症中最常见的事件之一，可用于断开对细胞生长的控制，外源性生长刺激的存活和新陈代谢。在这里，我们讨论了我们目前对控制PI3K和AKT下游细胞代谢的分子事件以及这些事件如何结合癌症的两个主要特征的理解：通过致癌信号的生长因子独立性和支持细胞存活和增殖的代谢重编程。