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Varisli, Lokman; Ozturk, Bilge E.; Akyuz, Gencer K.; Korkmaz, Kemal S.
<?xml version='1.0' encoding='utf-8'?> <oai_dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd"> <dc:creator>Varisli, Lokman</dc:creator> <dc:creator>Ozturk, Bilge E.</dc:creator> <dc:creator>Akyuz, Gencer K.</dc:creator> <dc:creator>Korkmaz, Kemal S.</dc:creator> <dc:date>2015-01-01</dc:date> <dc:description>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.</dc:description> <dc:identifier>https://aperta.ulakbim.gov.trrecord/80041</dc:identifier> <dc:identifier>oai:zenodo.org:80041</dc:identifier> <dc:rights>info:eu-repo/semantics/openAccess</dc:rights> <dc:rights>http://www.opendefinition.org/licenses/cc-by</dc:rights> <dc:source>JOURNAL OF CELLULAR BIOCHEMISTRY 116(1) 170-178</dc:source> <dc:title>HN1 Negatively Influences the beta-Catenin/E-Cadherin Interaction, and Contributes to Migration in Prostate Cells</dc:title> <dc:type>info:eu-repo/semantics/article</dc:type> <dc:type>publication-article</dc:type> </oai_dc:dc>
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