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Mannose receptor (MR) is a highly conserved, single-pass type I transmembrane protein in the endocytic system, and it serves as a mannose receptor, mediating the uptake of newly glycosylated proteins. In addition to being expressed in the liver, MR is expressed in a variety of other tissues, including macrophages, leukocytes, dendritic cells, and tumor cells. MR has been shown to enhance the phagocytosis of tumor cells by macrophages in vitro, and the receptor may have a regulatory function in the surveillance of tumors. In the present study, we generated MR knock-out mice and found that the MR deficiency resulted in a significant reduction of the breast cancer cell line, MB-231, in vivo. The anti-tumor effect of the MR deficiency was not due to the change of the tumor cell behavior, such as proliferation and migration. In addition, we found that the tumor growth was regulated by the macrophage-to-tumor cell ratio rather than the direct effect of the tumor cells. Therefore, MR expressed in the tumor cells may have a role in promoting tumor growth via macrophages. The MR deficiency in mice also prevented the interaction of MR-positive MB-231 cells with bone marrow-derived macrophages (BMDM) and inhibited their phagocy ac619d1d87
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