Previously, it has been reported that HN1 is involved in cytoplasmic retention and degradation of androgen receptor in an AKT dependent manner. As HN1 is a hormone inducible gene, and has been shown that it is upregulated in various cancers, we studied the importance of HN1 function in -catenin signaling in prostate cancer cell line, PC-3 and mammary cancer cell line MDA-MB231. Here, we demonstrated that HN1 physically associates with GSK3/-catenin destruction complex and abundantly localizes to cytoplasm, especially when the GSK3 is phosphorylated on S9 residue. Further, ectopic HN1 expression results an increase in the -catenin degradation leading to loss of E-cadherin interaction, concurrently contributing to actin re-organization, colony formation and migration in cancer cell lines. Thus, we report that HN1 is an essential factor for -catenin turnover and signaling, augments cell growth and migration in prostate cancer cells. J. Cell. Biochem. 116: 170-178, 2015. (c) 2014 Wiley Periodicals, Inc.