Related Experiment Video
Updated: Apr 21, 2026

08:54
An Immunofluorescent Method for Characterization of Barrett’s Esophagus Cells
Published on: July 20, 2014
13.1K
Eps8 controls Src- and FAK-dependent phenotypes in squamous carcinoma cells
Christina Schoenherr1, Bryan Serrels1, Charlotte Proby2
1Edinburgh Cancer Research Centre, Institute of Genetics and Molecular Medicine, University of Edinburgh, Crewe Road South, EH4 2XR Edinburgh, UK.
Journal of Cell Science
|November 1, 2014
Summary
Eps8 protein regulates Src and focal adhesion kinase (FAK) localization in squamous cell carcinoma (SCC). It controls Src trafficking to autophagic structures or focal adhesions, impacting SCC cell invasion and migration.
Area of Science:
- Cell Biology
- Cancer Research
- Molecular Biology
Background:
- Eps8 is an actin regulatory protein with elevated expression in squamous cell carcinoma (SCC).
- Eps8 interacts with focal adhesion kinase (FAK) and Src in SCC cells, particularly in the DMBA/TPA chemical carcinogenesis model.
Purpose of the Study:
- To elucidate novel roles of Eps8 in regulating the spatial distribution and function of Src and FAK in SCC.
- To understand how Eps8 modulates SCC cell invasion and migration through its interactions with FAK and Src.
Main Methods:
- Investigated Eps8's role in controlling active Src localization in SCC cells.
- Examined the FAK-dependent and FAK-absent mechanisms of Src trafficking mediated by Eps8.
- Assessed the requirement of Eps8 for FAK-dependent SCC cell polarization and invasion.
Main Results:
- Eps8 controls active Src spatial distribution in a FAK-dependent manner.
- In FAK-absent SCC cells, Eps8 drives Src trafficking to autophagic structures.
- In FAK-expressing SCC cells, Eps8 localizes to focal adhesions and is essential for FAK-dependent polarization and invasion.
Conclusions:
- Eps8 is a critical mediator of Src and FAK functions in SCC.
- Eps8 regulates actin rearrangements, influencing Src localization and modulating FAK/Src-driven invasive migration.
- Eps8 plays a dual role in SCC cell behavior, affecting both autophagic coping mechanisms and invasive processes.

