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目的观察0.8 kb的Mucin 1黏蛋白(MUC1)启动子驱动人钠/碘同向转运体(hNIS)基因在胰腺癌细胞靶向表达,评估其吸收碘的能力及结合放射碘治疗胰腺癌的效果。方法采用双质粒脂质体共转染方法获得复制缺陷型腺病毒Ad/MUC1/hNIS。Ad/MUC1/hNIS体外感染细胞,通过免疫荧光染色方法及细胞~(125)I的吸收试验检测hNIS在细胞的靶向表达及吸碘功能。构建鼠Capan-2胰腺癌模型,瘤内注射病毒后,结合~(131)I治疗,观察对移植瘤生长的抑制作用。结果hNIS仅在MUC1阳性的CAPAN-2和SW1990细胞的胞膜靶向表达,且有高的~(125)I吸收能力,分别较对照组提高20.5和13倍。Ad/MUC1/hNIS感染的肿瘤结合~(131)I治疗能抑制肿瘤生长,肿瘤体积减小到原来的83%。结论0.8 kb的MUC1启动子能驱动hNIS基因在MUC1阳性的胰腺癌细胞靶向表达,结合~(131)I治疗后能抑制胰腺癌的生长。
Objective To observe the targeted expression of the human sodium / iodine symporter (hNIS), a 0.8 kb Mucin 1 mucin (MUC1) promoter, in pancreatic cancer cells to assess its ability to absorb iodine and the effect of radioiodine in pancreatic cancer . Methods The replication-deficient adenovirus Ad / MUC1 / hNIS was obtained by double-plasmid liposome co-transfection. The cells were infected with Ad / MUC1 / hNIS in vitro, and the expression of hNIS in cells and the function of iodine uptake were detected by immunofluorescence staining and cell uptake assay. The mouse model of pancreatic cancer of Capan-2 was established. After intratumoral injection of virus, combined with ~ (131) I treatment, the inhibitory effect on the growth of the transplanted tumor was observed. Results hNIS was only expressed on the membrane of MUC1-positive CAPAN-2 and SW1990 cells, and had a high absorption capacity of 125I, which was 20.5 and 13 times higher than that of the control group. Tumor combined with ~ (131) I treatment infected with Ad / MUC1 / hNIS inhibited tumor growth and reduced the tumor volume to 83%. Conclusion The 0.8 kb MUC1 promoter can drive hNIS gene expression in MUC1 positive pancreatic cancer cells. Combined with ~ (131) I treatment, it can inhibit the growth of pancreatic cancer.