Document Detail


δ-Catenin promotes E-cadherin processing and activates β-catenin-mediated signaling: implications on human prostate cancer progression.
MedLine Citation:
PMID:  22261283     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
δ-Catenin binds the juxtamembrane domain of E-cadherin and is known to be overexpressed in some human tumors. However, the functions of δ-catenin in epithelial cells and carcinomas remain elusive. We found that prostate cancer cells overexpressing δ-catenin show an increase in multi-layer growth in culture. In these cells, δ-catenin colocalizes with E-cadherin at the plasma membrane, and the E-cadherin processing is noticeably elevated. E-Cadherin processing induced by δ-catenin is serum-dependent and requires MMP- and PS-1/γ-secretase-mediated activities. A deletion mutant of δ-catenin that deprives the ability of δ-catenin to bind E-cadherin or to recruit PS-1 to E-cadherin totally abolishes the δ-catenin-induced E-cadherin processing and the multi-layer growth of the cells. In addition, prostate cancer cells overexpressing δ-catenin display an elevated total β-catenin level and increase its nuclear distribution, resulting in the activation of β-catenin/LEF-1-mediated transcription and their downstream target genes as well as androgen receptor-mediated transcription. Indeed, human prostate tumor xenograft in nude mice, which is derived from cells overexpressing δ-catenin, shows increased β-catenin nuclear localization and more rapid growth rates. Moreover, the metastatic xenograft tumor weights positively correlate with the level of 29kD E-cadherin fragment, and primary human prostate tumor tissues also show elevated levels of δ-catenin expression and the E-cadherin processing. Taken together, these results suggest that δ-catenin plays an important role in prostate cancer progression through inducing E-cadherin processing and thereby activating β-catenin-mediated oncogenic signals.
Authors:
Hangun Kim; Yongfeng He; Ilhwan Yang; Yan Zeng; Yonghee Kim; Young-Woo Seo; Mary Jo Murnane; Chaeyong Jung; Jae-Hyuk Lee; Jeong-Joon Min; Dong-Deuk Kwon; Kyung Keun Kim; Qun Lu; Kwonseop Kim
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2012-01-11
Journal Detail:
Title:  Biochimica et biophysica acta     Volume:  1822     ISSN:  0006-3002     ISO Abbreviation:  Biochim. Biophys. Acta     Publication Date:  2012 Apr 
Date Detail:
Created Date:  2012-03-05     Completed Date:  2012-09-24     Revised Date:  2014-04-30    
Medline Journal Info:
Nlm Unique ID:  0217513     Medline TA:  Biochim Biophys Acta     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  509-21     Citation Subset:  IM    
Copyright Information:
Copyright © 2012 Elsevier B.V. All rights reserved.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cadherins / metabolism*
Catenins / physiology*
Cell Line, Tumor
Disease Progression
Humans
Male
Mice
Mice, Nude
Prostatic Neoplasms / pathology*
Protein Processing, Post-Translational*
Signal Transduction / physiology*
beta Catenin / physiology*
Grant Support
ID/Acronym/Agency:
R01 CA111891/CA/NCI NIH HHS; R01 CA111891-02/CA/NCI NIH HHS; R01 CA111891-03/CA/NCI NIH HHS; R01 CA111891-04/CA/NCI NIH HHS; R01 CA111891-04S1/CA/NCI NIH HHS; R01CA111891/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Cadherins; 0/Catenins; 0/beta Catenin; 0/delta catenin
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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