LKB1 tumor suppressor protein: PARtaker in cell polarity

The LKB1 (also called serine/threonine kinase 11) tumor suppressor gene was cloned in 1998 by linkage analysis of Peutz-Jeghers cancer syndrome patients. Mammalian LKB1 has been implicated as a regulator of multiple biological processes and signaling pathways, including the control of cell-cycle arr...

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Bibliographic Details
Published in:	Trends in cell biology 2004-06, Vol.14 (6), p.312-319
Main Authors:	Baas, Annette F, Smit, Linda, Clevers, Hans
Format:	Article
Language:	eng
Subjects:	Animals Caenorhabditis elegans Caenorhabditis elegans Proteins - genetics Caenorhabditis elegans Proteins - physiology Cell Polarity - genetics Cell Polarity - physiology Drosophila Drosophila Proteins - genetics Drosophila Proteins - physiology Humans Models, Biological Protein-Serine-Threonine Kinases - genetics Protein-Serine-Threonine Kinases - physiology Sequence Homology, Amino Acid Signal Transduction - physiology Tumor Suppressor Proteins - genetics Tumor Suppressor Proteins - physiology
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Summary:	The LKB1 (also called serine/threonine kinase 11) tumor suppressor gene was cloned in 1998 by linkage analysis of Peutz-Jeghers cancer syndrome patients. Mammalian LKB1 has been implicated as a regulator of multiple biological processes and signaling pathways, including the control of cell-cycle arrest, p53-mediated apoptosis, Wnt signaling, transforming growth factor (TGF)-beta signaling, ras-induced cell transformation, and energy metabolism. The Caenorhabditis elegans and Drosophila melanogaster LKB1 homologs, termed PAR4 and dLKB1, respectively, regulate cell polarity. Recently, mammalian LKB1 was found to be active only in a complex with two other proteins--STRAD and MO25--and to induce complete polarization of intestinal epithelial cells in a cell-autonomous fashion. In this article, we summarize the findings regarding LKB1 over the past six years. In addition, we discuss LKB1 in polarity in the context of both the other PAR proteins and its tumor suppressive activities.
ISSN:	0962-8924 1879-3088