Similarly, silencing BCAS2 with shRNA led to reduced nuclear β-catenin in the human colon cancer cell line SW480, in which β-catenin was activated because of mutations in the adenomatous polyposis coli protein (APC), an integral component of the β-catenin destruction complex (Figure 4F, Rosin-Arbesfeld et al., 2003). This evidence concerns the gene BCAS2 and colonic neoplasm.