Related Experiment Video
Updated: Apr 20, 2026

Characterization of Cell Membrane Extensions and Studying Their Roles in Cancer Cell Adhesion Dynamics
Published on: March 26, 2018
Focal adhesion kinase-regulated signaling events in human cancer
Abstract:
Abstract Focal adhesion kinase (FAK) is a non-receptor protein tyrosine kinase that is highly expressed or activated in many human cancers. Under specific scenarios, FAK can regulate cell proliferation, cell survival, cell migration and invasion, and has been implicated in the control of tumorigenesis and metastasis. FAK has both catalytic and scaffolding activity, and triggers downstream signals by activation of a number of pathways, including the Ras/mitogen-activated protein kinase pathway, the phosphatidylinositol 3'-kinase/Akt pathway, and Rho family GTPases. Recent evidence also suggests novel signaling interactions between FAK and p53. These signaling events were defined primarily from studies on cells in culture, and elucidating which of these signaling pathways are pathologically relevant downstream of FAK in human cancer remains an important goal in determining the molecular mechanisms of tumorigenesis and metastasis. This review discusses select evidence of these signaling pathways with an emphasis on studies linking these to animal models of cancer and human disease. The role of FAK in the process of epithelial-to-mesenchymal transition and in cancer stem cells and recent therapeutic advances targeting FAK are also discussed.
Insights
Focal adhesion kinase (FAK) plays a key role in cancer progression by regulating cell growth, movement, and invasion. Understanding FAK
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase implicated in numerous human cancers.
- FAK regulates critical cellular processes including proliferation, survival, migration, invasion, tumorigenesis, and metastasis.
- FAK possesses both catalytic and scaffolding functions, influencing downstream signaling pathways.
Purpose of the Study:
- To review signaling pathways downstream of FAK in cancer.
- To emphasize studies linking FAK signaling to animal cancer models and human disease.
- To discuss FAK's role in epithelial-to-mesenchymal transition, cancer stem cells, and therapeutic strategies.
Main Methods:
- Literature review of studies on FAK signaling in cancer.
- Emphasis on evidence from animal models and human disease.
- Discussion of FAK's involvement in epithelial-to-mesenchymal transition and cancer stem cells.
Main Results:
- FAK activates key pathways such as Ras/MAPK, PI3K/Akt, and Rho GTPases.
- Novel signaling interactions between FAK and p53 are emerging.
- FAK is linked to epithelial-to-mesenchymal transition and cancer stem cell properties.
Conclusions:
- Elucidating FAK's pathological signaling in human cancer is crucial for understanding tumorigenesis and metastasis.
- FAK is a significant target for cancer therapy, with recent therapeutic advances showing promise.
- Further research into FAK-mediated pathways can lead to novel anti-cancer strategies.
Related Concept Videos
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
mTOR Signaling and Cancer Progression
Intracellular Signaling Affects Focal Adhesions
Some...
Interactions Between Signaling Pathways
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
MAPK Signaling Cascades
PI3K/mTOR/AKT Signaling Pathway

