论文部分内容阅读
目的:研究选择性环氧化酶-2(COX-2)抑制剂塞来昔布联合氟尿嘧啶对胰腺癌细胞株SW1990生长的抑制作用,并对其机制进行初步探讨。方法:实验分为对照组、氟尿嘧啶组、塞来昔布组及两药联合组,将不同浓度的药物分别作用于胰腺癌细胞株SW1990,MTT法检测各组细胞的生长抑制率,并探索产生最佳细胞生长抑制作用的药物浓度。流式细胞仪检测不同药物作用对肿瘤细胞周期的影响。RT-PCR检测各组细胞Survivin的表达情况。结果:MTT法显示氟尿嘧啶、塞来昔布均能抑制SW1990的生长,且细胞的存活率都随药物浓度的增加而降低。两药联合组对细胞生长的抑制作用更明显。流式细胞仪检测结果显示塞来昔布组、氟尿嘧啶组及两药联合组细胞较对照组G0/G1期细胞比例明显增加,S期和G2/M期细胞比例明显减少。RT-PCR结果显示氟尿嘧啶组、塞来昔布组、联合组都可下调Survivin的表达,以联合组最为明显。结论:塞来昔布联合氟尿嘧啶对胰腺癌SW1990细胞的生长具有抑制作用,其机制可能与下调Survivin的表达从而诱导细胞的凋亡和细胞周期的停滞有关。
AIM: To investigate the inhibitory effect of selective cyclooxygenase-2 (COX-2) inhibitor celecoxib combined with 5-fluorouracil on the growth of pancreatic cancer cell line SW1990 and its mechanism. Methods: The experiment was divided into control group, fluorouracil group, celecoxib group and combination of two drugs, different concentrations of drugs were applied to the pancreatic cancer cell line SW1990, MTT assay to detect the growth inhibition rate of each group of cells, and to explore the production Optimal cytostatic effect of drug concentration. Flow Cytometry to detect the effect of different drugs on tumor cell cycle. Survivin expression in each group was detected by RT-PCR. Results: MTT assay showed that both fluorouracil and celecoxib could inhibit the growth of SW1990, and the cell viability decreased with the increase of drug concentration. Combination of two drugs on cell growth inhibition is more obvious. Flow cytometry results showed that the proportion of cells in the celecoxib group, the fluorouracil group and the two drug combination group was significantly increased compared with the control group at G0 / G1 phase, and the proportion of cells in S phase and G2 / M phase was significantly decreased. The result of RT-PCR showed that the expression of Survivin in fluorouracil group, celecoxib group and combination group were down-regulated, which was the most obvious in combination group. CONCLUSION: Celecoxib combined with 5-fluorouracil inhibits the growth of pancreatic cancer cell line SW1990. The mechanism may be related to the down-regulation of Survivin expression and the induction of cell apoptosis and cell cycle arrest.