Document Detail


NIP1/DUOXA1 expression in epithelial breast cancer cells: regulation of cell adhesion and actin dynamics.
MedLine Citation:
PMID:  19322654     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
DUOXA1/NIP1, originally identified as a Numb-interacting protein, was recently shown to function as a maturation factor for the dual oxidase 1(DUOX1). In this study, we identified DUOXA1/NIP1 expression in breast cancer cells, observed high expression of DUOXA1 in non-invasive MCF7 cells and low expression in highly metastatic cells with impaired p53 functions linking the expression of DUOXA1 with p53. An inhibition of cell proliferation associated with upregulation of p21(Cip1/WAF1) was observed in MDA-MB-231 cells following transfection of DUOXA1. The transient DUOXA1 overexpression also inhibited expression of cell-surface integrin alphaVbeta5 and CD9, which is associated with impaired spreading ability. However, there was no difference in expression of these proteins in DUOX1-depleted cells. The observed effects coincided with an increase in reactive oxygen species (ROS) generation. Our data also demonstrate that DUOXA1 transient overexpression affected the cell-cell adhesion by modulating the actin cytoskeleton, and sensitized cells to doxorubicin.
Authors:
Elena A Ostrakhovitch; Shawn S C Li
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-03-26
Journal Detail:
Title:  Breast cancer research and treatment     Volume:  119     ISSN:  1573-7217     ISO Abbreviation:  Breast Cancer Res. Treat.     Publication Date:  2010 Feb 
Date Detail:
Created Date:  2010-01-14     Completed Date:  2010-03-23     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8111104     Medline TA:  Breast Cancer Res Treat     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  773-86     Citation Subset:  IM    
Affiliation:
Department of Biochemistry and Siebens Drake Medical Research Institute, Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON N6A 5C1, Canada. eostrakh@uwo.ca
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MeSH Terms
Descriptor/Qualifier:
Actins / metabolism*
Blotting, Western
Breast Neoplasms / genetics,  metabolism*
Cell Adhesion / physiology
Cell Line, Tumor
Cell Separation
Cyclin-Dependent Kinase Inhibitor p21 / genetics,  metabolism
Cytoskeleton / metabolism
Epithelial Cells / metabolism
Female
Flow Cytometry
Fluorescent Antibody Technique
Gene Expression
Gene Expression Regulation, Neoplastic / genetics*
Humans
NADPH Oxidase
Nuclear Cap-Binding Protein Complex / biosynthesis*,  genetics
Reactive Oxygen Species / metabolism
Reverse Transcriptase Polymerase Chain Reaction
Transfection
Tumor Suppressor Protein p53 / genetics,  metabolism
Grant Support
ID/Acronym/Agency:
//Canadian Institutes of Health Research
Chemical
Reg. No./Substance:
0/Actins; 0/Cyclin-Dependent Kinase Inhibitor p21; 0/NCBP2 protein, human; 0/Nuclear Cap-Binding Protein Complex; 0/Reactive Oxygen Species; 0/Tumor Suppressor Protein p53; EC 1.6.3.1/DUOX1 protein, human; EC 1.6.3.1/NADPH Oxidase

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


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