Inhibition of cell migration, spreading, and focal adhesions by tumor suppressor PTEN
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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Previous studies described downregulation of focal adhesion formations in NIH3T3 cell lines engineered to overexpress PTEN, in apparent contradiction to the effect shown here, where the same effect resulted from PTEN loss.
“These studies described the downregulation of focal adhesion formations in NIH3T3 cell lines engineered to overexpress PTEN, in apparent contradiction to the effect shown here, where the same effect resulted from PTEN loss.”
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“Illustratively, the involvement of PTEN in the focal adhesion pathway via direct regulation of focal adhesion kinase (FAK; PTK2) has been reported (Tamura et al., 1998, 1999).”
- Authors
- Tamura, M., Gu, J., Matsumoto, K., Aota, S.-I., Parsons, R., & Yamada, K. M.
- Affiliations
- National Institutes of Health (US)
- Corresponding author
- Tamura, Masahito
- Yamada, Kenneth M.
- Venue
- Science
- Published
- 1998-06-05
- Volume
- 280
- Issue
- 5369
- Pages
- 1614-1617
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W2076457965
- Cited by
- 1,215
- References
- 0
- Citations by year
- 2026: 8 · 2025: 16 · 2024: 17 · 2023: 24 · 2022: 18 · 2021: 22 · 2020: 27 · 2019: 32 · 2018: 38 · 2017: 34 · 2016: 34 · 2015: 47 · 2014: 39 · 2013: 43 · 2012: 44
- FWCI
- 36.02
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Immunology and Allergy › Cell Adhesion Molecules Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Keywords
- PTEN, tumor suppressor, cell migration, cell spreading, focal adhesions, integrin signaling, focal adhesion kinase, tyrosine phosphorylation, phosphatase activity, tensin, extracellular matrix
- MeSH terms
- Animals, Cell Adhesion, Cell Line, Cell Movement, Concanavalin A, Ecdysone, Fibronectins, Humans, Mutation, Phosphoric Monoester Hydrolases, Phosphorylation, Polylysine, Protein-Tyrosine Kinases, Recombinant Proteins, Transfection, Tumor Cells, Cultured, Signal Transduction, Down-Regulation, Cell Adhesion Molecules, Integrins, Genes, Tumor Suppressor, 3T3 Cells, Protein Tyrosine Phosphatases, Tumor Suppressor Proteins, Cell Size, PTEN Phosphohydrolase, Mice, Focal Adhesion Protein-Tyrosine Kinases, Focal Adhesion Kinase 1
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