We’ve rebranded some of our products, learn more ›

CODEX® is now PhenoCycler,
Phenoptics™ is now Phenolmager.

MicroRNA-200c restoration reveals a cytokine profile to enhance M1 macrophage polarization in breast cancer

Authors: Williams, Michelle M.; Christenson, Jessica L.; O’Neill, Kathleen I.; Hafeez, Sabrina A.; Ihle, Claire L.; Spoelstra, Nicole S.; Slansky, Jill E.; Richer, Jennifer K.

Online: http://www.nature.com/articles/s41523-021-00273-1

Issue: NPJ Breast Cancer. 2021 May 27;7(1):64.


Many immune suppressive mechanisms utilized by triple negative breast cancer (TNBC) are regulated by oncogenic epithelial-to-mesenchymal transition (EMT). How TNBC EMT impacts innate immune cells is not fully understood. To determine how TNBC suppresses antitumor macrophages, we used microRNA-200c (miR-200c), a powerful repressor of EMT, to drive mesenchymal-like mouse mammary carcinoma and human TNBC cells toward a more epithelial state. MiR-200c restoration significantly decreased growth of mouse mammary carcinoma Met-1 cells in culture and in vivo. Cytokine profiling of Met-1 and human BT549 cells revealed that miR-200c upregulated cytokines, such as granulocyte-macrophage colony-stimulating factor (GM-CSF), promoted M1 antitumor macrophage polarization. Cytokines upregulated by miR-200c correlated with an epithelial gene signature and M1 macrophage polarization in BC patients and predicted a more favorable overall survival for TNBC patients. Our findings demonstrate that immunogenic cytokines (e.g., GM-CSF) are suppressed in aggressive TNBC, warranting further investigation of cytokine-based therapies to limit disease recurrence.