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目的研究抗肿瘤药物阿糖胞苷(Ara-C)与顺铂(DDP)联用,或单独使用抗肿瘤药物,作用于具有顺铂耐药性的TW03/DDP鼻咽癌细胞,探讨细胞生长抑制和凋亡的差异及可能机制。方法体外培养TW03/DDP细胞,运用实时定量PCR和Western blot法检测细胞中肺耐药相关蛋白(LRP)的表达;Ara-C与DDP联用或单独使用处理TW03/DDP细胞和不具耐药性的TW03鼻咽癌细胞后,运用CCK-8法检测其生长抑制率,流式细胞术检测其凋亡率。结果相对于TW03细胞,TW03/DDP细胞中LRP蛋白表达升高;Ara-C与DDP单独使用均能抑制TW03/DDP细胞和TW03细胞的生长并诱导凋亡,但DDP对TW03/DDP细胞作用弱;Ara-C与DDP联用可抑制以上两种细胞的生长,抑制率和凋亡率均大于二者单独应用的效果。结论Ara-C与DDP联用可以增强对耐药性鼻咽癌细胞的生长抑制作用和凋亡诱导作用。
Objective To study the antitumor effect of Ara-C combined with cisplatin (DDP) or antineoplastic agents alone in cisplatin-resistant TW03 / DDP nasopharyngeal carcinoma cells to explore the role of cell growth Differences and possible mechanisms of inhibition and apoptosis. Methods TW03 / DDP cells were cultured in vitro. The expression of lung resistance-related protein (LRP) in cells was detected by real-time PCR and Western blot. Ara-C cells were treated with DDP alone or without drug resistance Of TW03 nasopharyngeal carcinoma cells, using CCK-8 method to detect the growth inhibition rate, flow cytometry to detect the apoptosis rate. Results Compared with TW03 cells, the expression of LRP protein in TW03 / DDP cells was increased. Both Ara-C and DDP alone inhibited the growth of TW03 / DDP cells and TW03 cells and induced apoptosis, but the effect of DDP on TW03 / DDP cells was weak Ara-C combined with DDP can inhibit the growth of the above two kinds of cells, the inhibition rate and the apoptosis rate are greater than the effect of the two alone. Conclusion Ara-C combined with DDP can enhance the growth inhibition and apoptosis induction of drug-resistant nasopharyngeal carcinoma cells.