论文部分内容阅读
目的:研究甲基化抑制剂5-氮杂-2’-脱氧胞苷(5-Aza-CdR)对人胃肠道间质瘤细胞GIST882生物学行为的影响,探讨其临床治疗胃肠道间质瘤的可能性。方法:MTT法和软琼脂集落形成实验检测5-Aza-CdR对GIST882细胞增殖的影响,划痕愈合及Transwell小室实验观察细胞体外迁徙侵袭能力的改变,流式细胞术检测5-Aza-CdR对细胞凋亡和细胞周期的影响,免疫细胞化学检测处理前后Caspase-9和Bcl-2蛋白表达的变化。结果:5-Aza-CdR呈浓度和时间依赖性抑制GIST882细胞增殖,并减弱GIST882细胞的迁移及侵袭能力,P<0.05。药物作用48h后,10ng/mL时细胞凋亡率为(7.4±0.8)%,与对照组相比显著升高,P<0.05;100ng/mL时G0/G1期细胞比例显著增加,细胞周期阻滞于G0/G1期。经5-Aza-CdR作用后,凋亡相关蛋白Caspase-9的表达增加,Bcl-2的表达降低,P<0.05。结论:5-Aza-CdR能抑制胃肠道间质瘤GIST882细胞增殖,诱导其凋亡,具有一定的临床应用前景。中华肿瘤防治杂志,2011,18(12):912-916
Objective: To investigate the effect of methylation inhibitor 5-aza-2’-deoxycytidine (5-Aza-CdR) on the biological behavior of GIST882 in human gastrointestinal stromal cells Tumor possibility. Methods: The proliferation of GIST882 cells was detected by MTT assay and soft agar assay. Scratch healing and Transwell chamber assay were used to observe the migration and invasion of cells in vitro. Flow cytometry was used to detect 5-Aza-CdR Apoptosis and cell cycle. The changes of Caspase-9 and Bcl-2 protein expression before and after immunocytochemistry were detected. Results: 5-Aza-CdR could inhibit the proliferation of GIST882 cells in a concentration-and time-dependent manner and attenuate the migration and invasion of GIST882 cells (P <0.05). After 48h treatment, the apoptotic rate was (7.4 ± 0.8)% at 10ng / mL, significantly higher than that of the control group (P <0.05). The proportion of cells in G0 / G1 phase increased significantly at 100ng / mL, Lag in G0 / G1 period. After 5-Aza-CdR treatment, the expression of Caspase-9 and Bcl-2 were decreased (P <0.05). CONCLUSION: 5-Aza-CdR can inhibit the proliferation and induce apoptosis of GIST882 cells in gastrointestinal stromal tumors. It has certain clinical application prospects. Chinese Journal of Cancer Prevention and Treatment, 2011,18 (12): 912-916