The Focal Adhesion Kinase‐‐A Regulator of Cell Migration and Invasion

@article{Hauck2002TheFA,
  title={The Focal Adhesion Kinase‐‐A Regulator of Cell Migration and Invasion},
  author={Christof R. Hauck and Datsun A. Hsia and David D. Schlaepfer},
  journal={IUBMB Life},
  year={2002},
  volume={53}
}
Cell migration plays an important role in embryonic development, wound healing, immune responses, and in pathological phenomena such as tissue invasion and metastasis formation. In this review, we summarize recent reports that connect the focal adhesion kinase (FAK) to cell migration and invasion. FAK is a nonreceptor protein tyrosine kinase involved in signal transduction from integrin‐enriched focal adhesion sites that mediate cell contact with the extracellular matrix. Multiple protein… 
[The characteristics of focal adhesion kinase (FAK) and its role in carcinogenesis].
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The evaluation of FAK expression in cancer cells might become an important prognostic factor, sinceFAK expression studies provide important information that provides the opportunity to identify the cancer grade.
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TLDR
Evidence has emerged directly linking FAK expression to tumour development in vivo, raising the possibility that intervention strategies to block FAK function may potentially provide an opportunity for the development of anticancer therapeutics.
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TLDR
It is suggested that FAK and Pyk2 function as important signaling effectors in gliomas and indicate that their differential regulation may be determining factors in the temporal development of proliferative or migrational phenotypes.
Heparin plays a key regulatory role via a p53/FAK‐dependent signaling in melanoma cell adhesion and migration
TLDR
The results of this study clearly demonstrate that the action of heparin in the regulation of melanoma cell adhesion and migration involves a p53/FAK/signaling pathway, which may be of importance in molecular targeted therapy of the disease.
Protein Kinase C-δ and Protein Kinase C-ε Cooperatively Enhance Epithelial Cell Spreading via Transactivation of Epidermal Growth Factor Receptor and Actin-Dependent Phosphorylation of Focal Adhesion-Associated Proteins
TLDR
The involvement of the PKC signaling pathway in regulation of epithelial cell motility is investigated and siRNA-mediated down-regulation of PKCδ and PKCε, but not PKCα, significantly attenuated cell spreading, indicating that two novel isoforms PKC δ andPKCε are the critical elements participating inregulation of epithelium cell spreading.
Focal adhesion kinase (FAK) activation by estrogens involves GPER in triple-negative breast cancer cells
TLDR
It is found that estrogenic GPER signaling triggers Y397 FAK phosphorylation as well as the increase of focal adhesion points (FAs) in TNBC cells, and FAK inhibition prevents the migration of T NBC cells upon GPER activation.
Understanding the Roles of FAK in Cancer
TLDR
FAK inhibitors as well as genetic mouse models are discussed to provide mechanistic insights into FAK signaling and its potential in cancer therapy.
Inhibition of focal adhesion kinase induces apoptosis in human osteosarcoma SAOS-2 cells
TLDR
The current data support evidence that down-regulation of FAK could induce SAOS-2 apoptosis through the caspase-dependent cell death pathway and may be important for therapies designed to enhance the apoptosis in osteosarcoma.
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References

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FAK integrates growth-factor and integrin signals to promote cell migration
Here we show that cells lacking focal adhesion kinase (FAK) are refractory to motility signals from platelet-derived and epidermal growth factors (PDGF and EGF respectively), and that stable
Alterations in the focal adhesion kinase/Src signal transduction pathway correlate with increased migratory capacity of prostate carcinoma cells
Focal adhesion kinase (FAK) has been implicated in the regulation of cell migration. In addition, FAK expression is increased in a number of highly metastatic tumor cell lines. Therefore, we
Required role of focal adhesion kinase (FAK) for integrin-stimulated cell migration.
TLDR
It is shown that stable re-expression of epitope-tagged FAK reversed the morphological defects of the FAK- cells through the dynamic regulation of actin structures and focal contact sites in fibronectin (FN) stimulated cells.
Inhibition of focal adhesion kinase expression or activity disrupts epidermal growth factor-stimulated signaling promoting the migration of invasive human carcinoma cells.
TLDR
Comparisons between normal, FAK-null, andFAK-reconstituted fibroblasts revealed that FAK enhanced EGF-stimulated JNK and ERK2 kinase activation that was required for cell motility, and support a role for inhibitors of FAK expression or activity in the control of neoplastic cell invasion.
Focal adhesion kinase is involved in mechanosensing during fibroblast migration
TLDR
The results suggest that FAK plays an important role in the response of migrating cells to mechanical input, and suggest that phosphorylation at Tyr-397 is required for some, but not all, of the functions of FAK in cell migration.
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TLDR
Two distinct, additive pathways regulating cell migration that are downregulated by tumor suppressor PTEN are identified: one involves Shc, a MAP kinase pathway, and random migration, whereas the other involves FAK, p130Cas, more extensive actin cytoskeletal organization, focal contacts, and directionally persistent cell motility.
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  • L. Cary, J. Guan
  • Biology
    Frontiers in bioscience : a journal and virtual library
  • 1999
TLDR
Focal adhesion kinase's roles in the regulation of several integrin-mediated cellular events are discussed, including the promotion of cell migration, proliferation and spreading, and the prevention of cell apoptosis.
Focal adhesion kinase and its potential involvement in tumor invasion and metastasis
Integrins are cell surface receptors which, in part, mediate the adhesion of cells to the extracelluar matrix. In addition to providing a molecular “glue” essential for tissue organization and
Induced Focal Adhesion Kinase (FAK) Expression in FAK-Null Cells Enhances Cell Spreading and Migration Requiring Both Auto- and Activation Loop Phosphorylation Sites and Inhibits Adhesion-Dependent Tyrosine Phosphorylation of Pyk2
TLDR
It is demonstrated that both the FAK autophosphorylation and activation loop sites are critical for maximum adhesion-induced FAK activation and FAK-enhanced cell spreading and migration responses.
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