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目的探索ｐ１６基因在脑胶质瘤发生发展过程中的作用及其与脑胶质瘤细胞顺铂化疗敏感性的关系。方法采用脂质转染的方法．将外源野生型ｐ１６基因导入胶质瘤细胞株Ｕ２５１，观察ｐ１６基因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，对转染后细胞生长情况、细胞周期及细胞对顺铂（ｃｉｓ－ｄｉａｍｍｉｎｅｄｉｃｈｌｏｒｏｐｌａｔｉｎｕｍ，ＣＤＤＰ）敏感性的变化进行分析。结果外源ｐ１６基因的高水平表达显著掏了胶质瘤Ｕ２５１细胞的生长，克隆形成率减少，克隆形成率减少，肿瘤细胞发生了Ｇ１期阻滞，同时，细胞对顺铂的敏感性降低，化疗药物诱导的凋亡细胞数减少。结论外源野生型ｐ１６基因可抑制胶质瘤细胞恶性增殖，同时降低Ｕ２５１细胞对顺铂的化疗敏感性。ｐ１６基因转染后对顺铂诱导凋亡作用的抑制可能是其主要机制。
Objective To explore the role of p16 gene in the development of glioma and its relationship with chemosensitivity of glioma cells to cisplatin. Methods Lipofection method was used. The exogenous wild-type p16 gene was introduced into glioma cell line U251 to observe the effect of long-term stable transfection of p16 gene on glioma cells and to screen positive clones. At the same time, empty vector plasmid PCDNA3 was used as control. The expression of p16 gene was detected by immunohistochemistry and Northern blotting. The changes of cell growth, cell cycle and sensitivity to cis-diamminedichloroplatinum (CDDP) after transfection were analyzed. Results The high level expression of exogenous p16 gene significantly increased the growth of glioma U251 cells. The rate of colony formation was reduced, the rate of colony formation was reduced, and G1 phase arrest was observed in tumor cells. At the same time, the sensitivity of cells to cisplatin was decreased, Chemotherapy induced a decrease in the number of apoptotic cells. Conclusion Exogenous wild-type p16 gene can inhibit malignant proliferation of glioma cells and reduce chemosensitivity of U251 cells to cisplatin. Inhibition of cisplatin-induced apoptosis after p16 gene transfection may be the main mechanism.