Down-regulation of p120 occurs frequently in colon, prostate, breast, lung, and other carcinoma types (for review see Thoreson and Reynolds, 2002), but the consequences are unknown. Paradoxically, it is rare to see p120 down-regulation in established tumor cell lines. The lone exception is the SW48 colon carcinoma cell line, where genetic alterations result in extremely low levels of a mutated p120 that lacks the carboxy terminus (Ireton et al., 2002). Restoring normal levels of full-length p120 expression in these poorly organized cells stabilized E-cadherin and caused a striking rescue of epithelial morphology. Thus, in SW48 cells at least, p120 appears to be essential for E-cadherin stability and function (Ireton et al., 2002). On the other hand, recent reports in Drosophila (Myster et al., 2003; Pacquelet et al., 2003) and Caenorhabditis elegans (Pettitt et al., 2003) indicate that p120 is not essential, and that its absence causes only minor defects that are not fully apparent unless complemented by weak alleles of E-cadherin or α-catenin.
