Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 23, Issue 2, Pages -Publisher
MDPI
DOI: 10.3390/ijms23020974
Keywords
CD146; triple negative breast cancer; treatment
Funding
- INSERM, Aix-Marseille University
- MSD Avenir
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Over-expression of CD146 leads to increased secretion of sCD146 in TNBC cells, promoting TNBC development and dissemination through up-regulation of EMT and CSC markers. These effects can be blocked using specific anti-sCD146 antibody, M2J-1 mAb. M2J-1 mAb is able to reduce tumor development and dissemination by affecting CSC.
Background: Triple Negative Breast Cancers (TNBC) are the most aggressive breast cancers and lead to poor prognoses. This is due to a high resistance to therapies, mainly because of the presence of Cancer Stem Cells (CSCs). Plasticity, a feature of CSCs, is acquired through the Epithelial to Mesenchymal Transition (EMT), a process that has been recently shown to be regulated by a key molecule, CD146. Of interest, CD146 is over-expressed in TNBC. Methods: The MDA-MB-231 TNBC cell line was used as a model to study the role of CD146 and its secreted soluble form (sCD146) in the development and dissemination of TNBC using in vitro and in vivo studies. Results: High expression of CD146 in a majority of MDA-MB-231 cells leads to an increased secretion of sCD146 that up-regulates the expression of EMT and CSC markers on the cells. These effects can be blocked with a specific anti-sCD146 antibody, M2J-1 mAb. M2J-1 mAb was able to reduce tumour development and dissemination in a model of cells xenografted in nude mice and an experimental model of metastasis, respectively, in part through its effects on CSC. Conclusion: We propose that M2J-1 mAb could be used as an additional therapeutic approach to fight TNBC.
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