Dialogue between LKB1 and AMPK: a hot topic at the cellular pole.
Dialogue between LKB1 and AMPK: a hot topic at the cellular pole.
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DOI：
10.1126/stke.4042007pe51
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发表时间：
2007-09-18
期刊：
影响因子：
--
通讯作者：
Billaud, Marc
中科院分区：
文献类型：
--
作者：
Forcet, Christelle;Billaud, Marc
细胞结构的破坏和能量代谢的改变是恶性细胞的两个特征。然而，很少有证据表明这两种癌症标志涉及共同信号通路的干扰。进入LKB 1，一种激酶，是肿瘤抑制因子，也是腺苷一磷酸（AMP）激活蛋白激酶（AMPK）的上游激活因子，AMPK是细胞能量状态的关键传感器。四项研究表明，LKB 1通过AMPK信号促进紧密连接的形成并维持上皮极性。因此，LKB1似乎是一类新型的肿瘤抑制因子，充当能量感应和极性检查点。
Disruption of cell architecture and change of energy metabolism are two traits of malignant cells. Yet, there was scant evidence that these two cancer hallmarks involved perturbations of a common signaling pathway. Enter LKB1, a kinase that is a tumor suppressor and that is an upstream activator of the adenosine monophosphate (AMP)-activated protein kinase (AMPK), a key sensor of cellular energy status. Four studies now reveal that LKB1 signals through AMPK to facilitate the formation of tight junctions and to maintain epithelial polarity. Thus, LKB1 appears to be a novel class of tumor suppressor that acts as an energy-sensing and polarity checkpoint.