论文部分内容阅读
目的 探索p16基因在脑胶质瘤发生发展过程中的作用及p16基因与肿瘤细胞放射敏感性间的关系。方法 将外源野生型p16基因导入胶质瘤细胞株U251、C6，筛选阳性克隆。同时以空载体质粒pCDNA3为对照，免疫组化检测p16基因表达，用MTT法测定细胞生长曲线及肿瘤杀伤率。结果 转染p16基因的U251、C6细胞有外源p16基因的整合及表达，克隆形成率减少，生长速度明显减慢，对辐射的敏感性增强。结论 导入外源野生型p16基因可抑制胶质瘤细胞恶性增殖，提高胶质瘤细胞对辐射的敏感性。
Objective To explore the role of p16 gene in the development of glioma and the relationship between p16 gene and radiosensitivity of tumor cells. Methods Wild type p16 gene was transfected into U251 and C6 glioma cell lines and the positive clones were screened. Meanwhile, vector pCDNA3 was used as a control, p16 gene expression was detected by immunohistochemistry, and cell growth curve and tumor killing rate were determined by MTT assay. Results Transfection of U251 and C6 cells transfected with p16 gene resulted in the integration and expression of exogenous p16 gene. The rate of clonal formation was reduced, the growth rate was significantly slowed, and the sensitivity to radiation was enhanced. Conclusion The introduction of exogenous wild-type p16 gene can inhibit the malignant proliferation of glioma cells and increase the radiosensitivity of glioma cells.