Abstract
The aim of this research was to establish an experimental metastatic model to study the influence of IL-3 on the process of metastasis. To this aim, we (1) compared the metastatic potential of a spontaneous murine sacroma, NFsa, and IL-3 gene-transfected tumor, Nfsa-IL3, to lung; (2) analyzed the immune responses induced by tumors; and (3) investigated the effects of NO on the processes of metastasis. The results show that the metastatic potential of NFsa was reduced by IL-3 gene transfection. Although the growth of NFsa tumors caused infiltration of macrophages, their cytotoxicity against tumors was inhibited by NFsa tumors. On the other hard, the expression of IL-3 could trigger acute-phase inflammatory responses prior to the development of tumor-associated inhibitory reaction. This dominant inflammatory reaction finally lead to the development of specific T cell response resulting in the final eradication of residual tumors and the development of long-term immunity. This study also shows that NO is only involved in the early process of a metastasis by the finding that the administration of iNOS inhibitor, AG, increased the number of NFsa-IL-3 lung colony. However, it did not affect the immunogenicity of NFsa-IL3 because these mice also developed long-term immunity.