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Combined therapy of multidrug‐resistant human lung cancer with anti‐P‐glycoprotein antibody and monocyte chemoattractant protein‐1 gene transduction: The possibility of immunological overcoming of multidrug resistance

We determined whether transduction of the monocyte chemoattractant protein‐I (MCP‐I) gene into MDR human lung cancer cells affected their tumorigenicity and sensitivity to antibody‐dependent cellular cytotoxicity (ADCC) reaction mediated by the anti‐P‐glycoprotein (P‐gp) monoclonal antibody MRK 16. The human MCP‐I gene inerted into an expression vector (BCMGSNeo) was transfected into MDR human small‐cell lung cancer (H69/VP) cells. Monocyte chemotactic activity was found in culture supernatants collected from MCP‐I‐transfected H69/VP cells, but not in supernatants of parent and mock‐transfected cells. In an in vitro experiment, recombinant MCP‐I did not affected monocytemediated ADCC against H69/VP cells when added to the monocyte culture in either the activation or the effector phase at sufficient concentrations to attract and activate monocytes. Tumorigenicity and growth rates of MCP‐I‐producing H69/VP cells in nude mice were similar to those of parental cells and mock‐transfected cells. However, systemic treatment with MRK16 was move effective in inhibiting the formation of tumors by MCP‐I‐gene‐transfected cells than by mock‐transfected cells. Systemic treatment with MRK16 also inhibited the growth of a mixture (1:1) of MCP‐I‐producing cells and mock‐transfected cells. These results suggest that combination therapy with MRK16 and MCP‐I gene transduction may be a useful immunological strategy to inhibit the growth of human MDR cancer cells expressng P‐gp. Int. J. Cancer 71:170–177, 1997. © 1997 Wiley‐Liss, Inc.