双丁酰环腺苷酸抑制甲状腺癌细胞株 FTC-133增殖

摘要

Objective To study the effect of dualdi butyryl cyclic AMP (dbcAMP)on the proliferation of FTC-133 cell line. Methods FTC-133 cells were normally cultured and divided into control group,dbcAMP treatment group (0.5,1.0,2.0 mmol/L). After FTC-133 cells were treated with dbcAMP (0.5,1.0,2.0 mmol/L)for 24 h or 48 h,the growth activity and growth curve was detected by MTT.Changes of the cell cycle were detected by flow cytometry.The mRNA and protein expression of Raf1 were measured by RT-qPCR and Western blotting.Results Compared with control group,the growth activity of FTC-133 cells was re-duced by different levels of dbcAMP in a dose-time dependence manner.The number of FTC-133 cells was decreased in the S phase and increased in the G2/M phase.The mRNA and protein expression of Raf1 of treatment group were both reduced compared with control group.Conclusion dbcAMP significantly reduced FTC-133 cells proliferation and promoted apoptosis,and which might be involoved by ERK MAPK signalling.%目的：探讨双丁酰环腺苷酸(dbcAMP)对甲状腺癌细胞株 FTC-133增殖的影响。方法将 FTC-133细胞进行常规培养,分为对照组,处理组(dbcAMP 0.5、1.0、2.0 mmol/L)共4组。采用四甲基偶氮唑蓝(MTT)法、生长曲线法观察0.5、1.0、2.0 mmol/L dbcAMP 经24 h、48 h 对甲状腺癌细胞株 FTC-133细胞增殖能力的影响,流式细胞术检测细胞周期的变化情况,使用反转录定量 PCR(RT-qPCR)和蛋白免疫印迹实验(Western Blotting)方法检测 Raf1的 mRNA 和蛋白表达水平。结果与对照组比较,不同浓度 dbcAMP 和时间处理的 FTC-133细胞增殖均受抑制,并表现出时间-剂量依赖性；S 期细胞显著减少,G2/M期细胞显著增加；Raf1 mRNA 和蛋白水平明显减低。结论dbcAMP 显著降低甲状腺癌细胞株 FTC-133的增殖能力,促进凋亡,可能与激活 ERK MAPK 通路有关。