Antitumor mechanism of mouse colon cancer cells transfected with IL-17 gene in vivo / 中国免疫学杂志

ABSTRACT

Objective:To investigate the effects of interleukin-17 on tumor,we transfected interleukin-17 gene into mouse colon cancer cells(C26)and set up an animal model in tumor.Methods:By plasmid vector,IL-17 gene was transfected into C26.Meanwhile, empty plasmid vector(pcDNA3.1)and C26 cells were transfected as control groups.C26/pcDNA3.1-IL-17,C26/pcDNA3.1,and C26 cells were subcutaneously inoculated into mice respectively and the tumor volume and the survival time were observed.Proliferation of splenocyte and NK activity were detected.Detect the characteristic cytokines and transcriptional factors of Th1,Th2,Th17 and Treg cells in splenic lymphocyte.Proliferation of TIL was detected.The characteristic cytokines IL-10 of M1 and the characteristic cytokines IL-12 of M2 in tumor infiltrating macrophages were detected.Results: The growth of tumor in mice inoculated with C26/pcDNA3.1-IL-17 cells was significantly retarded ( P0.05).The proliferation of the splenocytes from C26/pcDNA3.1-IL-17 inoculated mice was higher than those of C26/pcDNA3.1,C26 groups(P0.05),the proliferation of the splenocytes from C26/pcDNA3.1 and C26 inoculated mice was slow than those of normal groups(P0.05 ).The splenocytes from the mice inoculated with C26/pcDNA3.1-IL-17 cells secreted more IFN-γ( the characteristic cytokines of Th1 ) , IL-4 ( the characteristic cytokines of Th2),GATA-3,ROR-γt,IL-10(the characteristic cytokines of Treg)mRNA(P<0.05).The proliferation of TIL from C26/pcDNA3.1-IL-17 inoculated mice was higher than those of C26/pcDNA3.1,C26 groups(P<0.05),the proliferation of TIL from C26/pcDNA3.1-IL-17,C26/pcDNA3.1 and C26 inoculated mice was lower than those of normal groups( P<0.05).And there′s no differences among every groups of the express of cytokines IL-10 and IL-12 mRNA in tumor infiltrating macrophages(P<0.05).Conclusion: The transfection of IL-17 gene inhibited tumor growth in the mice,inoculated with enhancing the immune function.