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Updated: Aug 7, 2026

Impedance-based Real-time Measurement of Cancer Cell Migration and Invasion
Published on: April 2, 2020
New concepts regarding focal adhesion kinase promotion of cell migration and proliferation
Braden D Cox1, Meera Natarajan, Michelle R Stettner
1Department of Pathology, Division of Neuropathology, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA.
Abstract:
Focal adhesion kinase (FAK) is a non-receptor cytoplasmic tyrosine kinase that plays a key role in the regulation of proliferation and migration of normal and tumor cells. FAK associates with integrin receptors and recruits other molecules to the site of this interaction thus forming a signaling complex that transmits signals from the extracellular matrix to the cell cytoskeleton. Crk-associated substrate (CAS) family members appear to play a pivotal role in FAK regulation of cell migration. Cellular Src bound to FAK phosphorylates CAS proteins leading to the recruitment of a Crk family adaptor molecule and activation of a small GTPase and c-Jun N-terminal kinase (JNK) promoting membrane protrusion and cell migration. The relocalization of CAS and signaling through specific CAS family members appears to determine the outcome of this pathway. FAK also plays an important role in regulating cell cycle progression through transcriptional control of the cyclin D1 promoter by the Ets B and Kruppel-like factor 8 (KLF8) transcription factors. FAK regulation of cell cycle progression in tumor cells requires Erk activity, cyclin D1 transcription, and the cyclin-dependent kinase (cdk) inhibitor p27Kip1. The ability of FAK to integrate integrin and growth factor signals resulting in synergistic promotion of cell migration and proliferation, and its potential regulation by nuclear factor kappa B (NFkappaB) and p53 and a ubiquitously expressed inhibitory protein, suggest that it is remarkable in its capacity to integrate multiple extracellular and intracellular stimuli.
Insights
Focal adhesion kinase (FAK) regulates cell proliferation and migration by integrating extracellular signals. Its role in cell cycle progression and migration pathways highlights its importance in both normal and tumor cells.
Area of Science:
- Cell Biology
- Molecular Biology
- Cancer Research
Background:
- Focal adhesion kinase (FAK) is a cytoplasmic tyrosine kinase crucial for cell signaling.
- FAK connects the extracellular matrix to the cell cytoskeleton via integrin receptors.
- FAK influences cell proliferation and migration in normal and cancerous cells.
Purpose of the Study:
- To elucidate the multifaceted roles of FAK in regulating cell migration and proliferation.
- To understand FAK's integration of extracellular matrix and growth factor signals.
- To explore FAK's involvement in cell cycle control and its regulation by transcription factors.
Main Methods:
- The study reviews FAK's association with integrin receptors and signaling complexes.
- It examines the role of Crk-associated substrate (CAS) proteins in FAK-mediated cell migration.
- The research investigates FAK's transcriptional control of cyclin D1 and its regulation of cell cycle inhibitors like p27Kip1.
Main Results:
- FAK signaling, involving CAS proteins and c-Jun N-terminal kinase (JNK), promotes cell migration.
- FAK regulates cell cycle progression through transcriptional control of cyclin D1 via Ets B and KLF8.
- FAK integrates integrin and growth factor signals, synergistically promoting cell migration and proliferation.
Conclusions:
- FAK is a key integrator of diverse cellular signals, impacting fundamental processes like migration and proliferation.
- FAK's complex regulatory network, involving transcription factors and signaling molecules, underscores its significance in cell behavior.
- Understanding FAK's mechanisms offers potential therapeutic targets for cancer and other diseases.
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