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Starvation and Pseudo-Starvation as Drivers of Cancer Metastasis through Translation Reprogramming

机译：通过翻译重编程作为癌症转移的驱动程序的饥饿和伪饥饿

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Considerable progress has been made in identifying microenvironmental signals that effect the reversible phenotypic transitions underpinning the early steps in the metastatic cascade. However, although the general principles underlying metastatic dissemination have been broadly outlined, a common theme that unifies many of the triggers of invasive behavior in tumors has yet to emerge. Here we discuss how many diverse signals that induce invasion converge on the reprogramming of protein translation via phosphorylation of eIF2 alpha, a hallmark of the starvation response. These include starvation as a consequence of nutrient or oxygen limitation, or pseudo-starvation imposed by cell-extrinsic microenvironmental signals or by cell-intrinsic events, including oncogene activation. Since in response to resource limitation single-cell organisms undergo phenotypic transitions remarkably similar to those observed within tumors, we propose that a starvation/pseudo-starvation model to explain cancer progression provides an integrated and evolutionarily conserved conceptual framework to understand the progression of this complex disease.
机译：在鉴定微环境信号时，已经进行了相当大的进展，其影响可逆表型转变的支撑在转移级联中的早期步骤。然而，尽管大致概述了转移传播的一般原则，但统一肿瘤中侵入行为许多触发的共同主题尚未出现。在这里，我们讨论了通过EIF2α的磷酸化，饥饿反应的标志进行诱导诱导侵袭侵袭的不同信号。这些包括饥饿作为营养素或氧气限制的结果，或通过细胞外部微环境信号或细胞内在事件施加的伪饥饿，包括癌基因活化。由于响应于资源限制单细胞生物进行了表型过渡，从肿瘤内观察到的那些相似，我们提出了一种解释癌症进展的饥饿/伪饥饿模型提供了一个综合和进化的保守概念框架，以了解这一复杂的进展疾病。

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