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[Growth characteristics of a human myeloma cell line transfected with IL-6 cDNA]
T Takahashi1, Y Okuno, Y Ohsugi
1Second Department of Internal Medicine, Faculty of Medicine, Kyoto University.
It remains to be clarified whether IL-6 acts on the growth of human myeloma cells by an autocrine or paracrine mechanism. Even in established myeloma cell lines, the autocrine growth by IL-6 appears unusual. In the present study, we deviced a model of IL-6 autocrine growth in vitro by transfecting IL-6 cDNA into a human myeloma cell line that had a proliferative response to IL-6 but did not produce IL-6. After IL-6 transfection, the cells (S6B45) proliferated in culture media without IL-6. IL-6 production by S6B45 was demonstrated both at protein and mRNA level. The growth of S6B45 was definitely inhibited by anti-IL-6 (MH166) or anti-IL-6 receptor (PM1) monoclonal antibodies. Furthermore, S6B45 was successfully transplanted to nude mice. The transplanted tumor growth was clearly inhibited by the administration of MH166 or PM1 to the mice. The in vivo antitumor activity of these antibodies suggest a new therapeutic strategy against tumors that proliferate by an autocrine mechanism through a cytokine such as IL-6.
It remains to be clarified whether IL-6 acts on the growth of human myeloma cells by an autocrine or paracrine mechanism. Even in established myeloma cell lines, the autocrine growth by IL-6 appears unusual. In the present study, we deviced a model of IL-6 autocrine growth in vitro by transfecting IL-6 cDNA into a human myeloma cell line that had a proliferative response to IL-6 but did not produce IL-6. After IL-6 transfection, the cells (S6B45) proliferated in culture media without IL-6. IL-6 production by S6B45 was demonstrated both at protein and mRNA level. The growth of S6B45 was definitely inhibited by anti-IL-6 (MH166) or anti-IL-6 receptor (PM1) monoclonal antibodies. Furthermore, S6B45 was successfully transplanted to nude mice. The transplanted tumor growth was clearly inhibited by the administration of MH166 or PM1 to the mice. The in vivo antitumor activity of these antibodies suggest a new therapeutic strategy against tumors that proliferate by an autocrine mechanism through a cytokine such as IL-6.