title: [Inhibitory effect of IL-27 gene on tumor formation activity of Eca109 cells in nude mice and its mechanisms].
abstract: 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).
  
  
  CONCLUSIONS
  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.
authors.affiliation: Research Center, The Fourth Affiliated Hospital, Hebei Medical University/Hebei provincial Cancer Institute, Shijiazhuang, Hebei, PR China.
authors.forename: Li-Hua
authors.initials: LH
authors.lastname: Liu
authors.forename: Bao-En
authors.initials: BE
authors.lastname: Shan
authors.forename: Li-Li
authors.initials: LL
authors.lastname: Shao
authors.forename: Shi-Jie
authors.initials: SJ
authors.lastname: Wang
mesh_terms: D000818:Animals; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D004938:Esophageal Neoplasms / Q000378:metabolism / Q000473:pathology*; D053222:Fas Ligand Protein / Q000378:metabolism*; D005260:Female; D005822:Genetic Vectors; D006801:Humans; D007371:Interferon-gamma / Q000378:metabolism; D020381:Interleukin-17 / Q000235:genetics / Q000378:metabolism*; D016246:Lymphocytes, Tumor-Infiltrating / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D008819:Mice, Nude; D009368:Neoplasm Transplantation; D017452:Receptors, IgG / Q000378:metabolism; D012190:Retroviridae / Q000235:genetics; D015398:Signal Transduction; D014162:Transfection; D047368:Tumor Burden; D019014:fas Receptor / Q000378:metabolism*
chemical_list: D053222:Fas Ligand Protein; D020381:Interleukin-17; D017452:Receptors, IgG; D019014:fas Receptor; D007371:Interferon-gamma