Activation of focal adhesion kinase through an interaction with β4 integrin contributes to tumorigenicity of colon cancer

High expression of either beta 4 integrin or focal adhesion kinase (FAK) has been reported in human colon cancer. However, it remains unclear how beta 4 integrin together with FAK contributes to the tumorigenicity of colon cancer. Here, we demonstrate that the co-overexpression of beta 4 integrin and FAK positively correlates with advanced stages of human colon cancer. Activated beta 4 integrin interacts with FAK and subsequently induces FAK phosphorylation at Tyr397. Furthermore, ablation of the beta 4 integrin/FAK complex and/or FAK activation impair colon cancer cell proliferation, anchorage-independent growth, and tumorigenicity. Our data indicate that the beta 4 integrin/FAK complex and subsequent FAK activation are essential regulators during the tumorigenicity of colon cancer, and we suggest an alternative strategy for colon cancer therapy.