HN1 Negatively Influences the β‐Catenin/E‐Cadherin Interaction, and Contributes to Migration in Prostate Cells
- 28 August 2014
- journal article
- research article
- Published by Wiley in Journal of Cellular Biochemistry
- Vol. 116 (1), 170-178
- https://doi.org/10.1002/jcb.24956
Abstract
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. J. Cell. Biochem. 116: 170–178, 2015.Keywords
Funding Information
- TÜBİTAK (108S288, 110S134, 113Z083)
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