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Sci. STKE, 18 September 2007
Vol. 2007, Issue 404, p. pe51
[DOI: 10.1126/stke.4042007pe51]


Dialogue Between LKB1 and AMPK: A Hot Topic at the Cellular Pole

Christelle Forcet and Marc Billaud*

CNRS Unité Mixte de Recherche (UMR) 5201, Laboratoire de Génétique Moléculaire, Signalisation et Cancer, F-69008 Lyon, France; Université de Lyon, F-69003 Lyon, France; université Lyon 1, Domaine Rockefeller, F-69003 Lyon, France; Centre Léon Bérard, Lyon Cedex 08, Lyon, France.

Abstract: 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.

*Corresponding author: E-mail, billaud{at}

Citation: C. Forcet, M. Billaud, Dialogue Between LKB1 and AMPK: A Hot Topic at the Cellular Pole. Sci. STKE 2007, pe51 (2007).

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