脂质体介导CDKN2基因抑制肺癌细胞的实验研究

The Efficacy of CDKN2 Gene Mediated by A SA Liposome Vector On the Proliferation of Lung Cancer Cells

转染野生型CDKN2cDNA—SA脂质体复合物到NSCLC细胞系A549和SCLC细胞系SH77，用MTT方法测量细胞增殖活力，观察CDKN2基因是否能抑制非小细胞肺癌细胞的增殖。结果：SA阳离子脂质体介导CDKN2基因转染A549细胞后第1、3、5、8日OD值显著小于对照组（P＜0．01），而SH77细胞转染CDKN2基因后1、3、5、8日OD值与对照组比较无差别（P＞0．05）。在体外转染CDKN2基因能显著抑制NSCLC细胞增殖，对SCLC细胞无作用。结果表明肿瘤抑制基因CDKN2可望成为NSCLC基因替代治疗的候选基因。

Wild-type CDKN2 cDNA-Stearylamine(SA) cationic liposome complex was transfected into NSCLC cell line A549 cells and SCLC cell line SH77 cells, The proliferation of the cells was detected by MTT methods to examine whether CDKN2 gene inhibited the proliferation of non-small cell lung cancer (NSCLC) cell. Results showde: on days 1, 3, 5, 8 after CDKN2 gene transfection the OD values of A549 cells were obviously lower than those of control groups without CDKN2 gene transfection (P＜0. 01 ), while the OD values of SH77 cells showed no difference compared with the control groups (P＞0. 05 ). CDKN2 gene could significantly inhibit the proliferation of NSCLC cells and had little effect on SCLC cells in vitro. The observations suggest that the tumor suppressor gene CDKN2 is a potential candidate for ge ne replacement therapy of NSCLC.