A role for EMT in CD73 regulation in breast cancer

Meriem Hasmim; Guy Berchem; Bassam Janji

doi:10.1080/2162402X.2022.2152636

A role for EMT in CD73 regulation in breast cancer

Oncoimmunology. 2022 Nov 30;11(1):2152636. doi: 10.1080/2162402X.2022.2152636. eCollection 2022.

Authors

Meriem Hasmim¹, Guy Berchem^{1

2}, Bassam Janji¹

Affiliations

¹ Tumor Immunotherapy and Microenvironment Group, Department of Cancer Research, Luxembourg Institute of Health (LIH), Luxembourg City, Luxembourg.
² Department of Hemato-Oncology, Centre Hospitalier du Luxembourg, Luxembourg City, Luxembourg.

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; adenosine; epithelial-to-mesenchymal transition; immunotherapy; triple negative breast cancer.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Adenosine
Epithelial-Mesenchymal Transition*
Humans
Triple Negative Breast Neoplasms* / genetics

Substances

Adenosine

Grants and funding

This work was supported by grants from FNRS-Televie (7.4579.20-CD73), Luxembourg National Research Fund (BRIDGES2020/BM/15412275/SMART-COMBO; BRIDGES2021/BM/16358198/TRICK-ALDH and INTER/EUROSTARS21/16896480/C2I), Fondation Recherche Cancer et Sang, Luxembourg (INCOM BIOM), Kriibskrank Kanner Foundation; Luxembourg (Neuroimmunotherapy II-2019) and Stiftelsen Cancera (2022; Fonds De La Recherche Scientifique – FNRS).