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目的 :探讨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对鬼臼噻吩苷、顺铂化疗敏感性间的关系。方法 :将外源野生型p16基因导入胶质瘤细胞株U2 5 1,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。Northern杂交检测p16基因表达 ,对转染后细胞生长情况、细胞周期、裸鼠致瘤能力的变化及细胞对鬼臼噻吩苷和顺铂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抑制了胶质瘤U2 5 1细胞的生长 ,克隆形成率减少 ,肿瘤细胞发生了G1期阻滞 ,同时 ,细胞对鬼臼噻吩苷和顺铂的敏感性降低 ,其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 ,同时抑制了鬼臼噻吩苷和顺铂对U2 5 1细胞的诱导凋亡作用进而降低了U2 5 1细胞对鬼臼噻吩苷和顺铂的化疗敏感性。
Objective: To investigate the role of p16 gene in the development of glioma and its relationship with the susceptibility of ten glioma cell to docethenoosine and cisplatin. Methods: The wild-type p16 gene was introduced into glioma cell line U2 5 1 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. Northern blotting was used to detect the expression of p16 gene. The changes of cell growth, cell cycle, tumorigenicity in nude mice and the sensitivity of cell to teniposide and cisplatin were analyzed. Results: The high level expression of exogenous p16 gene significantly inhibited the growth of glioma U251 cells, decreased the rate of colony formation and arrested the G1 phase of tumor cells. Meanwhile, the cells were sensitive to teniposide and cisplatin Sex decreased, the number of induced apoptosis cells decreased. CONCLUSION: Exogenous wild-type p16 gene can inhibit malignant proliferation of glioma cells and inhibit the induction of apoptosis of U251 cells by notoginsengoside and cisplatin, Chemotherapy sensitivity of cisplatin.