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Tumor suppressor PTEN: modulator of cell signaling, growth, migration and apoptosis

Kenneth M. Yamada* and Masaru Araki

Craniofacial Developmental Biology and Regeneration Branch, National Institute of Dental and Craniofacial Research, Bethesda, MD 20892, USA



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  		Fig. 1. Major enzymatic function of PTEN. The tumor suppressor PTEN opposes the action of phosphoinositide 3-kinase (PI 3-kinase) by dephosphorylating the signaling lipid phosphatidylinositol (3,4,5)-trisphosphate.

 


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  		Fig. 2. Reported sites of action of PTEN. Extracellular interactions trigger signaling from integrins and growth factor receptors. The major function of PTEN appears to be downregulation of the PI 3-kinase product PtdIns(3,4,5)P3, which regulates Akt and complex downstream pathways affecting cell growth, survival and migration. In addition, PTEN has weak protein tyrosine phosphatase activity, which may target focal adhesion kinase (FAK) and Shc, and thereby modulate other complex pathways. The phosphatase domain of PTEN (red) dephosphorylates and downregulates (red lines) substrate molecules.

 


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  		Fig. 3. Regulation of cell migration by integrins, growth factors and PTEN. The signaling networks regulating the speed and directional persistence of migration can be dissected by PTEN reconstitution and overexpression of individual signaling molecules and mutants affecting specific steps in signal transduction pathways. These signaling networks modulate the directionality and speed of cell migration, which combine to govern overall cell migration.

 




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