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Department of Cancer Biology, University of Texas M. D. Anderson Cancer Center, Houston, TX 77030
We investigated the role of tumor cell-derived GM-CSF in
recruitment and tumoricidal activation of tissue macrophages.
Transfection of the murine GM-CSF gene into KM12SM human colon cancer
cells decreased the tumorigenicity of transfected cells and
nontransfected bystander colon cancer cells in nude mice. Sequential
tissue sections from sites injected with high GM-CSF-producing tumor
cells (but not from nontransfected or low GM-CSF-producing cells)
demonstrated a dense infiltration of polymorphonuclear cells (PMN),
followed by infiltration of macrophages, which correlated with
expression of the macrophage-inflammatory protein-1
and the monocyte
chemoattractant protein-1 (MCP-1) in mouse PMN and macrophages.
GM-CSF-producing KM12SM cells were highly sensitive to lysis by mouse
macrophages and also increased macrophage-mediated lysis of bystander
nontransfected KM12SM cells. The incubation of macrophages with GM-CSF
induced expression of the CD11b surface adhesion molecule, which was
associated with increased attachment to tumor cells. All KM12SM cells
were sensitive to macrophage-mediated lysis in the presence of rGM-CSF
and recombinant MCP-1. Collectively, the results demonstrate that tumor
cell-derived GM-CSF stimulates PMN and macrophages to secrete
macrophage-inflammatory protein-1 and MCP-1, which triggers
recruitment of mononuclear cells, induces expression of adhesion
molecules on macrophages, and enhances contact-dependent cytolysis of
tumor cells.
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