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目的 :观察c myc反义基因抑制人高转移性肺癌PG细胞增殖 ,下调侵袭黏附性的作用和机制。方法 :合成c myc反义寡核苷酸 ,经脂质体包裹 ,转导入c myc高表达的PG细胞中。RT PCR方法检测c mycmRNA表达水平的变化 ,流式细胞术检测c myc蛋白的表达。MTT法检测细胞增殖活性 ,黏附实验检测PG细胞的黏附性。结果 :c myc反义基因 (>0 .6 2 5μmol/L)对PG细胞c mycmRNA、蛋白表达和细胞增殖活性具有明显的抑制作用 ,其处理PG细胞 72h后 ,2 0～ 80min不同时间的细胞黏附百分率 ,从 5 0 .0 %,81.2 7%和 90 .0 %分别显著下降到 31.5 %,37.5 %和 30 .0 %(P <0 .0 5 ) ,下降呈时间依赖效应。结论 :c myc反义基因抑制PG细胞c mycmRNA和蛋白表达水平 ,同时下调增殖活性和侵袭黏附性。
OBJECTIVE: To observe the effect of c-myc antisense gene on PG cell proliferation and down-regulation of invasion and adhesion in human highly metastatic lung cancer. Methods: The c-myc antisense oligonucleotide was synthesized and encapsulated by liposome, and then transfected into PG cells with high expression of c-myc. RT-PCR method was used to detect the change of c mycmRNA expression. Flow cytometry was used to detect the expression of c-myc protein. MTT assay was used to detect cell proliferation activity. Adhesion assay was used to detect the adhesion of PG cells. Results: The c-myc antisense gene (> 0.655μmol / L) significantly inhibited the c-myc mRNA, protein expression and cell proliferation of PG cells. After treated with PG cells for 72h, the cells in different time from 20 to 80min The percentage of adhesion decreased significantly from 50.0%, 81.2% and 90.0% to 31.5%, 37.5% and 30.0% (P <0.05), respectively, with a time-dependent decrease. Conclusion: The c-myc antisense gene inhibits c-myc mRNA and protein expression in PG cells and down-regulates proliferative activity and invasion adhesion.