Our main findings were as follows: (1) 90K negatively regulates E-cadherin levels in a cell-population-dependent manner; (2) 90K affects the adhesive and motile properties of subconfluent cancer cells; (3) the 90K modulation of E-cadherin levels is mediated by ubiquitination-dependent proteasomal degradation; (4) 90K interacts with adherens junction proteins, which affects the phosphorylation status of p120-catenin and the association between p120-catenin and E-cadherin; and (5) 90K affects the cellular localization of p120-catenin. The gene discussed is CTNND1; the disease is cancer.