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Transfection of Macrophage Inflammatory Protein 1 into B16 F10 Melanoma Cells Inhibits Growth of Pulmonary Metastases But Not Subcutaneous Tumors¹

Hendrik W. van Deventer^2,*,, Jonathon S. Serody^*,, Karen P. McKinnon, Casey Clements, W. June Brickey^, and Jenny P.-Y. Ting^,

^* Division of Hematology/Oncology, Department of Medicine, Lineberger Comprehensive Cancer Center, and Department of Immunology and Microbiology, University of North Carolina, and University of North Carolina School of Medicine, Chapel Hill, NC 27599

Macrophage inflammatory protein 1 (MIP-1), a CC chemokine, is a chemoattractant for T cells and immature dendritic cells. Plasmacytoma cells expressing MIP-1 generate a cytotoxic T cell response without affecting tumor growth. To understand this discrepancy, we compared a local tumor model with a metastatic one using MIP-1-transfected B16 F10 melanoma cells. Clonal idiosyncrasies were controlled by selecting three lipotransfected tumor clones and two pcDNA vector transfected control clones with equivalent in vitro proliferative capacities. No significant differences were seen between the MIP-1-producing and control melanoma cells after s.c. injection in the hind leg. All animals had a leg diameter of 10 cm in 18.5–21.5 days. However, after i.v. injection the number of pulmonary foci was significantly reduced in the MIP-1-producing clones. Injection of 10⁶ control transfected cells resulted in a median of 98.5 tumor foci in 2 wk, whereas the injection of the MIP-1-producing clones resulted in 89.5, 26.5, and 0 foci. The number of metastatic foci was inversely proportional to the amount of MIP-1 produced by the clone in vitro. Flow cytometry showed a significant increase in CD8⁺ cells in lungs of mice with MIP-1-transfected tumors 3 days after injection. This increase was not maintained 10 days later despite continued production of MIP-1. The protection offered by transfection with MIP-1 was significantly impaired in ₂-microglobulin^-/- mice. Our findings suggest that MIP-1 is effective in preventing the initiation of metastasis, but not at sustaining an effective antitumor response.

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