M2a macrophages induce contact-dependent dispersion of carcinoma cell aggregates

Monocytes and macrophages accumulate at the site of tumors driven by chemokines such as CCL2, monocyte chemotactic protein 1 (MCP1), vascular endothelial growth factor (VEGF), and macrophage colony stimulating factor (M-CSF). Convincing evidence suggests that tumor-associated macrophages (TAMs) promote tumor growth, epithelial-mesenchymal transition (EMT) and intravasation of blood and lymph vessels. Recently, we reported experimental findings in a microfluidic tumor model demonstrating that M2a macrophages induce contact-dependent EMT of carcinoma cell aggregates via ICAM-1 and integrin β2 interactions. These findings support the pro-metastatic activities of M2a macrophages and may help in designing novel immunotherapies for cancer patients.