A role for EMT in CD73 regulation in breast cancer

Abstract

CD73 is an emerging target in cancer due to its role in generating adenosine, a potent immunosuppressor. We found that SNAI1, a driver of epithelial-to-mesenchymal transition (EMT), upregulates CD73 in triple negative breast cancer cells. Here, we discuss the relevance of improving CD73-based therapy by combining with inhibitors of EMT.

Keywords

• CD73
• SNAI1
• epithelial-to-mesenchymal transition
• adenosine
• triple negative breast cancer
• immunotherapy