Anti-esophageal cancer active immunity induced by FasL/B7-1 gene-modified tumor cells

This study aims to investigate the activation of CTLs against esophageal cancer cells induced by FasL/B7-1 (FB-11) gene-modified tumor cells, and to explore whether co-expression of FasL and B7-1 in Eca-109 tumor cells could initiate a synergistic antitumor effect. We found that FasL and B7-1-transfected cancer cells had a high apoptosis index; DNA laddering suggested that FasL and B7-1 genes induced esophageal cancer cell apoptosis. FasL(+)/B7-1(+) Eca-109 cells (Eca-109/FB-11) were inoculated subcutaneously in the dorsal skin of C57BL/6 mice, greatly decreasing their tumorigenicity (z = 2.15-46.10, P < 0.01). The Eca-109/FB-11 cell-sensitized mice obtained the protective immune activity against the re-challenge of wildtype Eca-109 cells (z = 2.06-44.30, P < 0.05). It was shown that the cytotoxicity of CTLs induced by Eca-109/FB-11 cells against Eca-109 was significantly higher than the one of CTLs activated by wild-type Eca-109 cells (84.1 +/- 2.4 vs 30.5 +/- 2.3%, P < 0.05). In conclusions, the results suggest that FasL and B7-1 can effectively promote the activity of CTLs against esophageal cancer cells, and FasL/B7-1 plays an important role in CTL cytotoxicity function as well. Ad-B7-1 also showed enhanced therapeutic efficiency for Eca-109 cells when combined with Ad-FasL.