Prevention of hepatocellular carcinoma in mice by IL-2 and B7-1 genes co-transfected liver cancer ce

来源 :World Journal of Gastroenterology | 被引量 : 0次 | 上传用户:civili
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AIM:To study the immunoprotective effect of liver cancervaccine with co-transfected IL-2 and B7-1 genes onhepatocarcinogenesis in mice.METHODS:The murine liver cancer cell line Hepal-6 wastransfected with IL-2 and/or B7-1 gene via recombinantadenoviral vectors and the liver cancer vaccines wereprepared.C57BL/6 mice were immunized with these vaccinesand challenged with the parental Hepal-6 cells afterwards.The immunoprotection was investigated and the reactive Tcell line was assayed.RESULTS:The immunoprotection of the tumor vaccine wasdemonstrated.The effect of IL-2 and B7-1 genes co-transfected Hepal-6 liver cancer vaccine(Hep6-IL2/B7vaccine)on the onset of tumor formation was the strongest.When attacked with wild Hepal-6 cells,the median survivalperiod of the mice immunized with Hep6-IL2/B7 vaccinewas the longest(68 days,χ~2=7.70-11.69,P<0.05)and theimplanted tumor was the smallest(z=3.20-44.10,P<0.05).The effect of single IL-2 or B7-1 gene-transfected vaccinewas next to the IL2/B7 gene co-transfected group,and themean survival periods were 59 and 54 days,respectively.The mean survival periods of wild or enhanced greenfluorescence protein gene modified vaccine immunized groupwere 51 and 48 days,respectively.The mice in control groupall died within 38 days and the implanted tumor was thelargest(z=3.20-40.21,P<0.05).The cellular immunofunctiontest and cytotoxicity study showed that the natural killer(NK)cell,lymphokine activated killer(LAK)cell and cytotoxicT lymphocyte(CTL)activities were significantly increased inmice immunized with the Hep6-IL2/B7 vaccine,(29.5±2.5 %,65.0±2.9 %,83.1±1.5 % respectively,compared with othergroups,P<0.05).CONCLUSION:The Hep6-IL2/B7 liver cancer vaccines caninduce the mice to produce activated and specific CTL againstthe parental tumor cells,and demonstrate stronger effecton the hepatocarcinogenesis than single gene modified orthe regular tumor vaccine.Therefore,the vaccines maybecome a novel potential therapy for recurrence andmetastasis of HCC. AIM: To study the immunoprotective effect of liver cancer virus with co-transfected IL-2 and B7-1 genes onhepatocarcinogenesis in mice. METHODS: The murine liver cancer cell line Hepal-6 wastransfected with IL-2 and / or B7-1 gene via recombinant adenovirus vectors and the liver cancer vaccines wereprepared. C57BL / 6 mice were immunized with these vaccines and challenged with the parental Hepal-6 cells afterwards. The immunoprotection was investigated and the reactive Tcell line was assayed .RESULTS: The immunoprotection of the tumor vaccine wasdemonstrated. The effect of IL-2 and B7-1 gene co-transfected Hepal-6 liver cancer vaccine (Hep6-IL2 / B7 vaccinia) on the onset of tumor formation was the strongest. When attacked with wild Hepal-6 cells, the median survival period of the mice immunized with Hep6-IL2 / B7 vaccine was the longest (68 days, χ ~ 2 = 7.70-11.69, P <0.05) and theimplanted tumor was the smallest IL-2 or B7-1 gene-transfected vaccinewas next to the IL2 / B7g ene co-transfected group, and themean survival periods were 59 and 54 days, respectively. The mean survival periods of wild or enhanced green fluid gene protein vaccine immunized group were 51 and 48 days, respectively. The mice in control group all died within 38 days and the cellular immunofunction test and cytotoxicity study showed that the natural killer (NK) cell, lymphokine activated killer (LAK) cell and cytotoxic T lymphocyte (CTL) activities were was increased increased (z = 3.20-40.21, inmice immunized with the Hep6-IL2 / B7 vaccine (29.5 ± 2.5%, 65.0 ± 2.9%, 83.1 ± 1.5% respectively, compared with other groups, P <0.05) .CONCLUSION: The Hep6-IL2 / B7 liver cancer vaccines caninduce the mice to produce activated and specific CTL against the parental tumor cells, and demonstrated stronger effecton the hepatocarcinogenesis than single gene modified orthe regular tumor vaccine. Before the, the vaccines maybecome a novel potential therapy for recurrence andmet astasis of HCC.
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