GReD Laboratory, CNRS UMR 6247, INSERM U931, Clermont Université, Faculté de Médecine, 63000 Clermont-Ferrand, France.
FEBS Lett. 2011 Apr 6;585(7):981-5. doi: 10.1016/j.febslet.2010.12.025. Epub 2010 Dec 23.
The LKB1 tumor suppressor kinase is an activator of the AMP-activated protein kinase (AMPK), a metabolic gauge that responds to variations of cellular energetic levels by favoring catabolic versus anabolic processes. Recent studies have provided substantial evidence that LKB1 and AMPK control cell polarity from invertebrates to mammals. This review examines how the LKB1-AMPK pathway, in conjunction with other positional signals, converts energy-sensing information into the activation of Myosin II to maintain epithelial-cell architecture but also to complete cell division. This molecular link between polarity and metabolism may constitute an ancient stress-response protective mechanism that was co-opted for tumor suppression during evolution.
LKB1 肿瘤抑制激酶是 AMP 激活的蛋白激酶 (AMPK) 的激活剂，AMPK 是一种代谢检测物，通过促进分解代谢而不是合成代谢来响应细胞能量水平的变化。最近的研究提供了大量证据表明，LKB1 和 AMPK 从无脊椎动物到哺乳动物控制细胞极性。这篇综述探讨了 LKB1-AMPK 途径如何与其他定位信号一起，将能量感应信息转化为肌球蛋白 II 的激活，以维持上皮细胞结构，但也完成细胞分裂。极性和代谢之间的这种分子联系可能构成一种古老的应激反应保护机制，在进化过程中被用于肿瘤抑制。
