p16基因抑制脑胶质瘤细胞恶性增殖并诱导细胞凋亡

目的：探索p16基因在脑胶质瘤发生过程中的作用及其与脑胶质瘤细胞凋亡的关系。方法：采用脂质体，磷酸钙＋DMSO休克转染的方法，分别将外源野生型p16基因导入胶质瘤细胞株U251，SWO，观察p16基因短暂转染与长期稳定转染对胶质瘤细胞的作用，并筛选阳性克隆。同时以空载体质粒pCDNA3为对照，免疫组化，Northern杂交检测p16基因表达，对转染后细胞生长的抑制，细胞周期，凋亡及裸鼠致瘤能力的变化进行分析，结果：外源p16基因的高水平表达显著抑制了胶质瘤U251，SWO细胞的生长，克隆形成率减少，肿瘤细胞发生了G1期阻滞，p16基因短暂转染可诱导胶质瘤细胞凋亡，而长期稳定转染无明显的凋亡诱导作用。结论：外源野生型p16基因可抑制胶质瘤细胞恶性增殖并诱导细胞凋亡，肿瘤细胞的异质性特点与p16基因转染后的“自然选择”作用可能是p16基因长期稳定转染无明显凋亡诱导作用的主要机制。

p16 Gene Inhibits Excessive proliferation of Glioma Cells and Induces Apoptosis of Glioma Cell Lines

Objective To explore the effect of p16 gene (CDK41) on the pathogenesis and development of human glioma and its relation to the glioma cell apoptosis. Methods By the method of lipofectin or calcium phosphate co-precipitation, p16 gene was transfected into glioma cell lines (U251 and SWO cells) and then the expression of exogenous p16 gene was determined by the techniques of immunohistochemistry and the Northern blot. The effects of exogenous p16 gene on the growth of U251 and SWO cells were examined in vivo and in vitro. Results The growth of U251 and SWO cells in vivo and in vitro was inhibited by the higher levels expression of exogenous p16 gene, and the cloning efficiencies of the two cell lines were reduced. Transient transfection of the exogenous p16 gene could induce the apoptosis of glioma cells, but its stable transfection could not. Conclusions The exogenous p16 gene could inhibit the glioma growth and induce the apoptosis of glioma cells.