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Updated: Mar 28, 2026
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Published on: September 18, 2013
Characterization of the expression of the pro-metastatic Mena(INV) isoform during breast tumor progression
Madeleine J Oudin1, Shannon K Hughes2,3, Nazanin Rohani2
1Koch Institute for Integrative Cancer Research, MIT, 76-317, 77 Massachusetts Ave, Cambridge, MA, 02139, USA. mjoudin@mit.edu.
Abstract:
Several functionally distinct isoforms of the actin regulatory Mena are produced by alternative splicing during tumor progression. Forced expression of the Mena(INV) isoform drives invasion, intravasation and metastasis. However, the abundance and distribution of endogenously expressed Mena(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(INV) isoform-specific monoclonal antibody and used it to examine Mena(INV) expression patterns in mouse mammary and human breast tumors. Mena(INV) expression increases during tumor progression and to examine the relationship between Mena(INV) expression and markers for epithelial or mesenchymal status, stemness, stromal cell types and hypoxic regions. Further, while Mena(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(INV)-isoform specific antibody, and provide the first description of endogenous Mena(INV) protein expression in mouse and human tumors.
Insights
Mena(INV) protein expression increases in mouse and human tumors during progression. This study developed a specific antibody to track Mena(INV) protein, revealing its distribution within tumors.
Area of Science:
- Molecular Biology
- Cancer Research
- Immunology
Background:
- Actin regulatory protein Mena exists in distinct isoforms produced by alternative splicing.
- The Mena(INV) isoform promotes tumor invasion, intravasation, and metastasis.
- Endogenous Mena(INV) protein abundance and distribution in primary tumors are largely unknown.
Purpose of the Study:
- To develop a specific monoclonal antibody for the Mena(INV) isoform.
- To investigate the expression patterns of endogenous Mena(INV) protein in mouse and human tumors.
- To correlate Mena(INV) expression with tumor progression and cellular markers.
Main Methods:
- Development of a Mena(INV) isoform-specific monoclonal antibody.
- Immunohistochemical analysis of Mena(INV) expression in mouse mammary and human breast tumors.
- Correlation analysis with markers for epithelial-mesenchymal status, stemness, stromal cells, and hypoxia.
Main Results:
- Mena(INV) protein expression significantly increases during tumor progression.
- Mena(INV) is robustly expressed in vascularized tumor areas but not exclusively confined to perivascular cells.
- The developed antibody demonstrates specificity and utility for detecting endogenous Mena(INV) protein.
Conclusions:
- This study provides the first description of endogenous Mena(INV) protein expression in tumors.
- Mena(INV) protein levels correlate with tumor progression.
- The findings highlight the role of Mena(INV) in the tumor microenvironment.
