Focal adhesion kinase (FAK) is a major integrin-dependent tyrosine phosphorylated protein, recently, FAK association with colorectal cancer (CRC) has gained attention. The various cancer-promoting mechanisms that associated with FAK can be implicated in the progression of CRC. The interactions between structural features of FAK and various kinases could be closely related to growth, survival, and metastasis in CRC cells. These interactions include human epithelial growth factor receptor, c-Met, platelet-derived growth factor receptor, vascular endothelial growth factor receptor, and Src. Such interactions can trigger the survival signaling of CRC cells and are also involved signaling downstream of phosphatidylinositol 3-kinase, AKT, and the extracellular regulated kinase. Based on this scientific background, many pharmaceutical companies are taking efforts to develop FAK inhibitors to treat solid cancer including CRC. Although the anti-cancer efficacies have been noted in many studies, the commercial drugs have not been developed yet. Therefore, the FAK research on CRC is expected to gain momentum and be highly appreciated as a potential field for developing the new drugs. Therefore, the studies on FAK that effect on the progression of human CRC s would be possible to suggest various approaches to CRC treatment, and FAK could be a potential target as an anticancer candidate for CRC therapies.
Keywords: Anticancer effect; Colorectal cancer; Focal adhesion kinase; Focal adhesion kinase inhibitor.