HN1 Negatively Influences the β‐Catenin/E‐Cadherin Interaction, and Contributes to Migration in Prostate Cells
Articles > Article · 2014
Authors: Lokman Varisli, Bilge Esin Öztürk, Gencer K. Akyuz, Kemal Sami KORKMAZ
Journal of Cellular Biochemistry, Journal Indexed in SCI Expanded, International, WoS, 2014, vol 116, pp 170-178
DOI: 10.1002/jcb.24956
Summary
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 β-catenin signaling in prostate cancer cell line, PC-3 and mammary cancer cell line MDA-MB231. Here, we demonstrated that HN1 physically associates with GSK3β/β-catenin destruction complex and abundantly localizes to cytoplasm, especially when the GSK3β is phosphorylated on S9 residue. Further, ectopic HN1 expression results an increase in the β-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 β-catenin turnover and signaling, augments cell growth and migration in prostate cancer cells.