Nanostring transcriptomic analysis of lungs from antiChemR23 treated and untreated 4T1-bearing mice

Macrophages are a major component of the tumor environment and their accumulation often correlates with poor prognosis and resistance to anticancer treatments. In this study, we thus investigated the therapeutic interest to target ChemR23, a receptor of the resolution of inflammation, in cancers using an agonist monoclonal antibody, antiChemR23. In vitro experiments on M2-like macrophages treated by antiChemR23 agonist decreased their inflammatory phenotype. In vivo, treatment with antiChemR23 agonist increased mouse survival and decreased metastasis occurrence in a model of triple-negative breast cancer in correlation with modulation of TAM phenotype in the metastatic niche. 4T1-luc2 cells (0.25x106/mouse in PBS) were injected into the fat pad of mammary gland of 8-week-old BALB/c female mice (day 0). Mice were treated with antiChemR23a agonist (n=7) or hIgG1 (n=4) mAbs intraperitoneally at 1mg/kg 3 times a week for 3 weeks from day 7 to day 28. At day 13, primary tumors were surgically removed from mammary glands. Tumor spreading was analyzed by overall survival and by in vivo bioluminescence on lungs every week using a bioimager.