Characterization of the expression of the pro-metastatic MenaINV isoform during breast tumor progression
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Author(s)
Rohani, Nazanin
Moufarrej, Mira N.
Jones, Joan G.
Condeelis, John S.
Gertler, Frank B.
Oudin, Madeleine Julie
Gertler, Frank
Hughes-Alford, Shannon Kay
Lauffenburger, Douglas A
Date Issued
December 2015
Journal
Clinical & Experimental Metastasis
Publisher
Springer Netherlands
Citation
Oudin, Madeleine J. et al. “Characterization of the Expression of the pro-Metastatic MenaINV Isoform during Breast Tumor Progression.” Clinical & Experimental Metastasis 33.3 (2016): 249–261.
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Author's final manuscript
Abstract
Several functionally distinct isoforms of the actin regulatory Mena are produced by alternative splicing during tumor progression. Forced expression of the Mena[superscript INV] isoform drives invasion, intravasation and metastasis. However, the abundance and distribution of endogenously expressed Mena[superscript INV] within primary tumors during progression remain unknown, as most studies to date have only assessed relative mRNA levels from dissociated tumor samples. We have developed a Mena[superscript INV] isoform-specific monoclonal antibody and used it to examine Mena[superscript INV]expression patterns in mouse mammary and human breast tumors. Mena[superscript INV] expression increases during tumor progression and to examine the relationship between Mena[superscript INV] expression and markers for epithelial or mesenchymal status, stemness, stromal cell types and hypoxic regions. Further, while Mena[superscript INV] robustly expressed in vascularized areas of the tumor, it is not confined to cells adjacent to blood vessels. Altogether, these data demonstrate the specificity and utility of the anti-Mena[superscript INV]-isoform specific antibody, and provide the first description of endogenous Mena[superscript INV]protein expression in mouse and human tumors.
MIT Department
Massachusetts Institute of Technology. Department of Biological Engineering
Massachusetts Institute of Technology. Department of Biology
Koch Institute for Integrative Cancer Research at MIT
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DOI of Published Version
https://doi.org/10.1007/s10585-015-9775-5
