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目的研究共转染人甲状腺过氧化物酶基因(hTPO)及人钠碘转运体基因(hNIS)后胶质瘤、肺癌及甲状腺癌细胞的摄碘能力变化。方法克隆、重组、包装并扩增纯化得到重组腺病毒(AdTPO),测定病毒滴度。使用脂质体转染法将hNIS基因转染入人胶质瘤、肺癌及甲状腺癌细胞系中,经过G418抗生素筛选获得稳定表达hNIS的细胞系,只转染hNIS基因的细胞系为对照组;应用重组腺病毒将hTPO基因传导入对照组中,共转染hNIS及hTPO基因的细胞系为实验组;未转入hTPO和hNIS基因的原始肿瘤细胞系为空白对照组。然后进行3组细胞系的体外摄125I率及各细胞系的125I外流实验。结果在各肿瘤细胞系中,实验组细胞的摄碘率和有效半衰期较对照组细胞及空白对照组细胞均有所提高,实验组细胞的摄碘率:H460组为59 628±1 281,U251组为7 968±1 261,ARO组为52 971±2 162,FRO组为49 638±1 281,3组间总体具有统计学差异(P<0.01)。结论将hTPO和hNIS基因共转染至肿瘤后能有效提高肿瘤的摄碘能力并延长细胞内碘滞留时间。
Objective To investigate the changes of iodine uptake of glioma, lung cancer and thyroid cancer cells after cotransfection of human thyroid peroxidase gene (hTPO) and human sodium iodide symporter gene (hNIS). Methods The recombinant adenovirus (AdTPO) was cloned, recombined, packaged and purified to determine the titer of the virus. The hNIS gene was transfected into human glioma, lung cancer, and thyroid cancer cell lines using liposome transfection method. The cell line stably expressing hNIS was obtained by G418 antibiotic screening, and the cell line transfected with hNIS gene was the control group. The hTPO gene was transduced into the control group using the recombinant adenovirus. The cell lines co-transfected with the hNIS and hTPO genes were used as the experimental group. The original tumor cell lines without hTPO and hNIS gene transfer were the blank control group. The in vitro rate of 125I in the three cell lines and the 125I efflux experiment in each cell line were then performed. Results In all tumor cell lines, the iodine uptake rate and effective half-life of cells in the experimental group were higher than those in the control group and the control group. The iodine uptake rate in the experimental group was 59 628±1 281 in the H460 group. The group was 7 968±1 261, the ARO group was 52 971±2 162, and the FRO group was 49 638±1 281. There was a statistically significant difference between the 3 groups (P<0.01). Conclusions Co-transfection of hTPO and hNIS genes into tumors can effectively increase the iodine uptake of tumors and prolong the intracellular iodine residence time.