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目的 探讨野生型 p5 3基因对顺铂诱导肿瘤细胞凋亡的影响。方法 用重组p5 3腺病毒 (Ad p5 3)和重组luc腺病毒 (Ad luc)分别感染 p5 3缺失的口腔癌细胞KB ,观察外源p5 3基因对顺铂诱导肿瘤细胞凋亡的影响。 结果 流式细胞术和原位末端标记显示用Ad luc与顺铂联合处理KB细胞不能诱导凋亡发生 ,用Ad p5 3与顺铂联合处理则诱导出较明显的细胞凋亡 ,表明p5 3可增强KB细胞对顺铂的敏感性 ;Northernblot显示 p5 3可下调bcl 2基因表达及上调bax基因的表达。结论 p5 3可能通过调节凋亡相关基因的表达水平而在顺铂诱导的肿瘤细胞凋亡中发挥重要作用 ,重组p5 3腺病毒与顺铂联合应用有助于克服 p5 3失活肿瘤细胞的耐药性。
Objective To investigate the effect of wild-type p53 gene on the apoptosis of tumor cells induced by cisplatin. Methods The p5 3-deleted oral cancer cells KB were infected with recombinant p5 3 adenovirus (Ad p5 3) and recombinant luc adenovirus (Ad luc) respectively and the effect of exogenous p5 3 gene on cisplatin-induced tumor cell apoptosis was observed. Results Flow cytometry and in situ end-labeling showed that KB cells treated with Ad-luc combined with cisplatin did not induce apoptosis. Combined treatment with Ad-p53 and cisplatin induced more significant apoptosis, indicating that p5 3 was Enhance the sensitivity of KB cells to cisplatin; Northernblot showed that p5 3 can down-regulate bcl 2 gene expression and up-regulate bax gene expression. Conclusion p5 3 may play an important role in cisplatin-induced tumor cell apoptosis by regulating the expression of apoptosis-related genes. Combined use of recombinant adenovirus p5 3 and cisplatin can help overcome the resistance of p5 3 -activated tumor cells Medicinal properties.