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

被引:1044
作者
Tamura, M
Gu, JG
Matsumoto, K
Aota, S
Parsons, R
Yamada, KM
机构
[1] NIDR, Craniofacial Dev Biol & Regenerat Branch, NIH, Bethesda, MD 20892 USA
[2] Columbia Univ Coll Phys & Surg, Dept Pathol, New York, NY 10032 USA
[3] Columbia Univ Coll Phys & Surg, Dept Med, New York, NY 10032 USA
关键词
D O I
10.1126/science.280.5369.1614
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
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.
引用
收藏
页码:1614 / 1617
页数:4
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