The Promotion of Metastasis through Interaction between MDSCs and B16F10 Melanoma

Abstract

Myeloid-derived suppressor cells (MDSCs) are heterogeneous immature myeloid cells that have an immunosuppressive function. Tumor cells take advantage of the tumor infiltrated MDSCs immunosuppressive function. In the tumor microenvironment (TME), MDSCs secrete several growth factors to facilitate tumor growth, angiogenesis, and metastasis. Milk fat globule epidermal growth factor 8 (MFG-E8) is one of the important factors having versatile roles in facilitating tumor growth, chemoresistance, cancer stem cell activation, and metastasis. In my study, I found that B16F10 melanoma cells secreted TGF-beta and TGF-beta treatment further increased the MFG-E8 expression in the MDSCs. In addition, MDSCs co-culture and MFG-E8 treatment increased migration activities of B16F10 cells. However, the increasing of migration activities by the MDSCs co-culture were blocked by neutralization of MFG-E8 with anti-MFG-E8 antibodies. Thus, my data suggest that the interaction between MDSCs and B16F10 cells promotes melanoma progression through the increasing of migration activities.