外源性血管抑素K(1-3)基因在人脑胶质瘤中的表达意义

目的 探讨外源性血和抑素Ｋ（１－３）基因「ａｎｇｉｏｓｔａｔｉｎＫ９１－３），ＡＫ（１－３）」在人脑胶质瘤中的表达及其作用。方法 应用ＰＣＲ法，使人Ｉｇｋａｐｐａ链分泌信号肽序列Ｓ中装在ＡＫ（１－３）基因上－ＳＡＫ（１－３）；构建ＳＡＫ（１－３）基因的真核表达载体ｐｃＤＮＡ－ＳＡＫ（１－３）。经脂质体法将其转染入ＳＨＧ４４人脑胶质瘤细胞，行Ｇ４１８筛选获得转基因瘤细胞克隆，比较转基因和内皮细胞抑制

Expression significance of extra-originated angiostatinK(1-3) gene in human gliomas

AIM To explore the expression and effects of extra originated angiostatin K(1 3) AK(1 3)] gene in human gliomas. METHODS AK(1 3) cDNA was linked with Ig kappa chain's secretive signal S to form SAK(1 3) by PCR. SAK(1 3) was inserted into polylinker sites of eukaryotic expression vector pcDNA3 to construct pcDNA SAK(1 3). The vector was transfected into human glioma SHG44 cells by lipofectamine and the positive clone was screened by G418. The biological characteristics of glioma cells before and after transfection were compared. The activity of AK(1 3) protein expressed by the SHG44 cells was examined by the endotheliocyte inhibition assay, immunofluorescence assay and immnohistochemistry. When the tumor cells were implanted into the nude mice, the influence of AK(1 3) protein to the human glioma growth was confirmed by some kind of tests. RESULTS The biological characteristics of glioma cells were not influenced by the extra originated AK(1 3) expression. The protein was able to inhibit the endothelial growth in vitro . The tumorigenesis of glioma cells in nude mice was greatly reduced and the tumor inhibition rate was 76.8%. CONCLUSION The human glioma growth can be withheld by the tumor's self expression of AK(1 3) protein. The mechanism is that the tumor angiogenesis is so suppressed that its necrosis happens.