Document Detail

PAX5alpha enhances the epithelial behavior of human mammary carcinoma cells.
MedLine Citation:
PMID:  20197384     Owner:  NLM     Status:  MEDLINE    
Deregulated PAX5 expression has been associated with metastatic mammary carcinoma, although the precise role of PAX5 in cancer progression is unclear. Stable forced expression of PAX5alpha in the mammary carcinoma cell lines MCF-7 and MDA-MB-231 reduced cell cycle progression, cell survival, and anchorage-independent cell growth. In xenograft studies, forced expression of PAX5alpha was associated with a significant reduction in tumor volume. Furthermore, forced expression of PAX5alpha in mammary carcinoma cells resulted in altered cell morphology with resultant enhancement of epithelial cell characteristics. Morphologic changes were associated with localization of beta-CATENIN at cell-cell junctions and with altered mRNA expression of mesenchymal markers in mammary carcinoma cells. In addition, forced expression of PAX5alpha in MCF-7 and MDA-MB-231 cells significantly reduced cell migration and invasion. Concomitantly, small interfering RNA-mediated depletion of PAX5alpha increased MCF-7 total cell number, cell motility, migration, and invasion. These studies show that PAX5alpha enhances the epithelial characteristics of mammary carcinoma cells, reminiscent of mesenchymal to epithelial transition.
Laurent J-P Vidal; Jo K Perry; Cecile M Vouyovitch; Vijay Pandey; Severine E Brunet-Dunand; Hichem C Mertani; Dong-Xu Liu; Peter E Lobie
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-03-02
Journal Detail:
Title:  Molecular cancer research : MCR     Volume:  8     ISSN:  1557-3125     ISO Abbreviation:  Mol. Cancer Res.     Publication Date:  2010 Mar 
Date Detail:
Created Date:  2010-03-18     Completed Date:  2010-07-12     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101150042     Medline TA:  Mol Cancer Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  444-56     Citation Subset:  IM    
The Liggins Institute, The University of Auckland, Auckland, New Zealand.
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MeSH Terms
B-Cell-Specific Activator Protein / genetics,  metabolism*
Biological Markers / metabolism
Breast Neoplasms / genetics,  metabolism*,  pathology
Carcinoma / genetics,  metabolism*,  pathology
Cell Count
Cell Dedifferentiation / physiology*
Cell Differentiation / genetics
Cell Line, Tumor
Cell Movement / genetics
Cell Transformation, Neoplastic / genetics,  metabolism
Down-Regulation / genetics
Epithelial Cells / cytology,  metabolism*
Gene Expression Regulation, Neoplastic / genetics
Intercellular Junctions / metabolism,  ultrastructure
Mesoderm / cytology,  metabolism
Neoplasm Invasiveness / genetics,  physiopathology
RNA Interference / physiology
RNA, Messenger / metabolism
Tumor Suppressor Proteins / genetics,  metabolism*
beta Catenin / metabolism
Reg. No./Substance:
0/B-Cell-Specific Activator Protein; 0/Biological Markers; 0/PAX5 protein, human; 0/RNA, Messenger; 0/Tumor Suppressor Proteins; 0/beta Catenin

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