[Inhibitory effect of IL-27 gene on tumor formation activity of Eca109 cells in nude mice and its mechanisms].

Background & Objective: Cytokine-based biotherapy is a hot spot in tumor research. This study was to explore the inhibitory effect of interleukin-27 (IL-27) on tumor formation activity of human esophageal carcinoma cell line Eca109 in nude mice, and investigate its antitumor mechanisms.
Methods: IL-27 gene was transfected into Eca109 cells with retrovirus vector and stable clones were selected by G418. The expression of IL-27 gene was detected by reverse transcription-polymerase chain reaction (RT-PCR). The secretion of IL-27 from Eca109/IL-27 cells and interferon-gamma (IFN-gamma) in peripheral blood mononuclear cells (PBMCs) were detected by ELISA. Cell proliferation in vitro was assessed by MTT assay. Eca109/IL-27, Eca109/LXSN and Eca109 cells were subcutaneously injected into nude mice to observe the growth of transplanted tumors. The expression of CD16 and FasL in tumor-infiltrating lymphocytes (TIL) and the expression of Fas in tumor cells were detected by flow cytometry.
Results: IL-27p28 and IL-27EBI3 were expressed in Eca109/IL-27 cells, but not in Eca109/LXSN and Eca109 cells (P<0.01). IL-27 secretion was significantly higher in Eca109/IL-27 cells than in Eca109/LXSN and Eca109 cells (P<0.01). The proliferation rates of the 3 cell lines were similar (P> 0.05). IFN-gamma secretion was significantly higher in Eca109/IL-27 cell-stimulated PBMCs than in Eca109/LXSN cell-and Eca109 cell-stimulated PBMCs [(56.28+/-1.61) pg/mL vs. (12.70+/-0.82) pg/mL and (11.06+/-0.64) pg/mL, P<0.01]. As compared with those in Eca109 and Eca109/LXSN groups, the tumor growth in nude mice was significantly slower in Eca109/IL-27 group (P<0.05), the expression of CD16 and FasL in TIL and the expression of Fas in tumor cells were up-regulated in Eca109/IL-27 group (P<0.05).
Conclusion: IL-27 gene may inhibit the tumor formation activity of Eca109 cells in nude mouse by activating natural killer (NK) cells through Fas/FasL pathway.