Forcet Christelle, Billaud Marc
CNRS Unité Mixte de Recherche 5201, Laboratoire de Génétique Moléculaire, Signalisation et Cancer, F-69008 Lyon, France.
Sci STKE. 2007 Sep 18;2007(404):pe51. doi: 10.1126/stke.4042007pe51.
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.
细胞结构破坏和能量代谢改变是恶性细胞的两个特征。然而，几乎没有证据表明这两个癌症标志涉及共同信号通路的扰动。肿瘤抑制激酶LKB1登场了，它是腺苷单磷酸（AMP）激活的蛋白激酶（AMPK）的上游激活剂，而AMPK是细胞能量状态的关键传感器。现在有四项研究表明，LKB1通过AMPK发出信号，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，可作为能量感应和极性检查点。
