Inhibition of Cell Migration, Spreading, and Focal Adhesions by Tumor Suppressor PTEN-Reference-Cited by-同舟云学术

Inhibition of Cell Migration, Spreading, and Focal Adhesions by Tumor Suppressor PTEN

Published:1998-06-05 Issue:5369 Volume:280 Page:1614-1617
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

Tamura Masahito¹²¹²,Gu Jianguo¹²¹²,Matsumoto Kazue¹²¹²,Aota Shin-ichi¹²¹²,Parsons Ramon¹²¹²,Yamada Kenneth M.¹²¹²

Affiliation:

1. M. Tamura, J. Gu, K. Matsumoto, S. Aota, K. M. Yamada, Craniofacial Developmental Biology and Regeneration Branch, National Institute of Dental Research, National Institutes of Health, Building 30, Room 421, 30 Convent Drive MSC 4370, Bethesda, MD 20892–4370, USA.

2. R. Parsons, Departments of Pathology and Medicine, College of Physicians and Surgeons, Columbia University, 630 West 168th Street, New York, NY 10032, USA.

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.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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