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HN1 Negatively Influences the β‐Catenin/E‐Cadherin Interaction, and Contributes to Migration in Prostate Cells
Author(s) -
Varisli Lokman,
Ozturk Bilge E.,
Akyuz Gencer K.,
Korkmaz Kemal S.
Publication year - 2015
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.24956
Subject(s) - protein kinase b , cytoplasm , microbiology and biotechnology , biology , cell culture , cancer research , nls , chemistry , phosphorylation , nuclear localization sequence , genetics
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. © 2014 Wiley Periodicals, Inc.