LKB1 Tumor Suppressor Protein: PARtaker in Cell Polarity

Trends Cell Biol. 2004 Jun;14(6):312-9. doi: 10.1016/j.tcb.2004.04.001.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • 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*

Substances

  • Caenorhabditis elegans Proteins
  • Drosophila Proteins
  • Tumor Suppressor Proteins
  • Stk11 protein, mouse
  • PAR-3 protein, C elegans
  • Protein-Serine-Threonine Kinases