RESUMO
Interferon y (IFN-?) could enhance the metastatic potential of a variety of tumors via increasing expression of MHC class I molecules or other unidentified mechanisms. It has been demonstrated that transfection of T-cell costimulatory molecule B7 gene into tumor cells could increase tumor immunogenicity and render them susceptible to immune attack. In this study, we investigate whether transfection of B7-1 gene could antagonize IFN-?-induced tumor metastasis. Lipofectamine-mediated transfection was used to introduce murine B7-1 (mB7-1) gene or neo gene into a low-metastatic variant of B16 melanoma cell line. The transfectants and parent B16 cells were treated with 100U/ml of IFN-? for 36 h before being subjected to experimental metastasis assay. The expression of MHC class I and class II molecules on the cells was analysed by flow cytometry. Pre-treatment of parent B16 cells and mock gene-transfected B16 cells (B16-neo) with IFN-? significantly increased their lung-metastizing capacity, while the same IFN-? treatment of B16 cells transfected with mB7-1 gene (B16-B7-1) showed no increase in the number of lung metastatic nodules as compared with control cells. Almost equally elevated expression of MHC class I (H-2Kb and H-2Db) molecules was found on the surface of B16, B16-neo and B16-B7-1 cells. However, a much higher expression of class II (I-Ab) molecule on B16-B7-1 cells than that on B16 and B16-neo cells was observed. These results demonstrate that transfection of B7-1 gene into B16 melanoma could reduce its IFN-?-induced metastasis and that the elevated MHC class II expression on B7-1-expressing cells might play a role in the B7-1 -associated reduction of metastasis.