简介：工程是调查IL-12基因的反肿瘤效果的这的目的修改了乳房的肉瘤鼠科的房间线，EMT6/IL-12，在里面老鼠模型。在这研究，我们transfectedrecombinant真核细胞的plasmid编码IL-12基因(pcDNA6-p70)进EMT6并且获得了表示EMT6/IL-12的IL-12房间线。当时，EMT6/IL-12房间是接种进老鼠的s.c。recombinant向量处理组被放作为控制。我们然后在象cytotoxicity，splenocytes的增长和连续IFN-水平那样的vivo评估了肿瘤生长和反肿瘤免疫功能的抑制。并且在splenocytes之中生产CD4或CD8T房间的IFN-的百分比也在忍受老鼠的肿瘤被分析。我们的结果证明肿瘤的生长显然在EMT6/IL-12组被禁止。而且，反肿瘤免疫的能力都在与控制相比的EMT6/IL-12组是显著地更高的。现在的调查的结果支持EMT6/IL-12能施加的观点在由改进反肿瘤的肿瘤模型的基因治疗细胞的免疫。

简介：ThepresentstudyisaimedatstudyingthegeneforTIMP-3,amammaliantissueinhibitor,byconstructingarecombinanteukaryoticcellvectorforgenetherapyinhumanbreastcancer.WeobtainedtheTIMP-3genefromthehumanplacentbyRT-PCR.TIMP-3genewassubclonedintopcDNA3.1vetorfrompMD18TvectorbymeansofgenecloningtoconstructpcDNA3.1recombinantvector.HumanbreastcancercelllineMDA-MB-453wastransfectedwithpcDNA3.1-TIMP3recombinantvectorusinglipofectaminereagent.ThentheexpressionofTIMP-3andtheeffectonthemetastasisofMDA-MB-453wereexamined.ThecorrectconstructionofpcDNA-TIMP3wasidentifiedbymeansofrestrictionenzymeanalysis,PCRamplicationandnucleotidesequencing.WesternblottingshowedthatthetransfectedcellswereabletoexpressTIMP-3,indicatingthatourconstructionofthepcDNA-TIMP3eukaryoticexpressionvectorwasconstructedsuccessfully.OurexperimentsfurtherindicatedthatthepotentialofmetastasiswassignificantlyreducedforthetransfectedcelllineMDA-MB-453.