Tai, Y.-L.Y.-L.TaiI-RUE LAIPeng, Y.-J.Y.-J.PengDing, S.-T.S.-T.DingTANG-LONG SHEN2020-02-272020-02-2720160014-5793https://www.scopus.com/inward/record.uri?eid=2-s2.0-84977599427&doi=10.1002%2f1873-3468.12215&partnerID=40&md5=30a01a3c97a0e7ae708c763e8105f36fhttps://scholars.lib.ntu.edu.tw/handle/123456789/465956High expression of either β4 integrin or focal adhesion kinase (FAK) has been reported in human colon cancer. However, it remains unclear how β4 integrin together with FAK contributes to the tumorigenicity of colon cancer. Here, we demonstrate that the co-overexpression of β4 integrin and FAK positively correlates with advanced stages of human colon cancer. Activated β4 integrin interacts with FAK and subsequently induces FAK phosphorylation at Tyr397. Furthermore, ablation of the β4 integrin/FAK complex and/or FAK activation impair colon cancer cell proliferation, anchorage-independent growth, and tumorigenicity. Our data indicate that the β4 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. ? 2016 Federation of European Biochemical Societies[SDGs]SDG3beta4 integrin; focal adhesion kinase; protein kinase B; amino terminal sequence; anchorage independent growth; animal experiment; animal model; autophosphorylation; biochemical analysis; cancer cell line; cancer growth; cancer staging; carcinogenicity; cell proliferation; Colo 205 cell line; colon cancer; colon carcinogenesis; complex formation; controlled study; disease association; embryo; enzyme activation; enzyme activity; enzyme phosphorylation; female; gene silencing; HCT116 cell line; HEK293 cell line; HeLa cell line; histopathology; human; human cell; human tissue; Letter; LoVo cell line; male; molecular dynamics; mouse; nonhuman; priority journal; protein expression; protein motif; protein protein interaction; SW480 cell lineletter10.1002/1873-3468.12215271787532-s2.0-84977599427