Paxillin-Y118 phosphorylation contributes to the control of Src-induced anchorage-independent growth by FAK and adhesion
2009
FAK and Src Interaction in Cancer Growth
publication
Evidence: moderate
Author Information
Author(s): Sanjay Sachdev, Yahao Bu, Irwin H. Gelman
Primary Institution: Roswell Park Cancer Institute
Hypothesis
How does FAK affect oncogenesis through the phosphorylation of Src substrates?
Conclusion
FAK influences the phosphorylation of Src substrates, affecting cancer cell growth and behavior.
Supporting Evidence
- FAK enhances Src-induced phosphorylation of certain substrates.
- Loss of FAK leads to increased anchorage-independent growth in cancer cells.
- Paxillin phosphorylation at Y118 is crucial for enhanced growth in the absence of FAK.
Takeaway
FAK helps control how cancer cells grow without needing to stick to surfaces, and when it's missing, certain signals can make them grow more freely.
Methodology
The study analyzed the phosphorylation profile of Src substrates in mouse embryo fibroblasts with and without FAK under different growth conditions.
Digital Object Identifier (DOI)
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