Characterization of the expression of the pro-metastatic MenaINV isoform during breast tumor progression
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 M...
Main Authors: | , , , , , , , , |
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Other Authors: | , , , , |
Format: | Article |
Language: | English |
Published: |
Springer Netherlands,
2016-07-14T21:18:56Z.
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Subjects: | |
Online Access: | Get fulltext |
Summary: | 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. United States. Dept. of Defense. Breast Cancer Research Program (Grants W81XWH-10-1-0040 and W81XWH-13-1-0031) National Institutes of Health (U.S.) (Grants U54-CA112967 and GM58801) Massachusetts Institute of Technology. Ludwig Center for Molecular Oncology |
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