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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: The exogenous wild-type p16 gene was introduced into glioma cell line U251, C6, screening positive clones. At the same time, empty vector plasmid was used as control, immunohistochemistry was used to detect the expression of p16 gene. Cell growth curve and tumor killing rate were determined by MTT assay. Results: U251 and C6 cells transfected with p16 gene had the integration and expression of exogenous p16 gene, the rate of clone formation decreased, the growth rate was slowed down, 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.