Inhibition of cell migration, spreading, and focal adhesions by tumor suppressor PTEN

Science. 1998 Jun 5;280(5369):1614-7. doi: 10.1126/science.280.5369.1614.

M Tamura ¹, J Gu, K Matsumoto, S Aota, R Parsons, K M Yamada

Affiliations

Affiliation

1 Craniofacial Developmental Biology and Regeneration Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, MD 20892-4370, USA. mtamura@yoda.nidr.nih.gov

PMID: 9616126 DOI: 10.1126/science.280.5369.1614

Abstract

The tumor suppressor PTEN is a Phosphatase with sequence similarity to the cytoskeletal protein tensin. Here the cellular roles of PTEN were investigated. Overexpression of PTEN inhibited cell migration, whereas antisense PTEN enhanced migration. Integrin-mediated cell spreading and the formation of focal adhesions were down-regulated by wild-type PTEN but not by PTEN with an inactive Phosphatase domain. PTEN interacted with the focal adhesion kinase FAK and reduced its tyrosine phosphorylation. Overexpression of FAK partially antagonized the effects of PTEN. Thus, PTEN Phosphatase may function as a tumor suppressor by negatively regulating cell interactions with the extracellular matrix.

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