摘要
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、2.0mmol/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、2.0mmol/L dbcAMP经24h、48h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;Raf1mRNA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。
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 retool/L）. After FTC-133 ceils were treated with dbcAMP （0.5,1.0,2.0 mmol/L） for 24 h or 48 h,the growth activity and growth eurve was detected by MTT. Changes of the cell cycle were detected by flow cytometry. The mRNA and protein expression of Rafl 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 Rafl 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.
出处
《重庆医学》
CAS
北大核心
2015年第24期3325-3327,共3页
Chongqing medicine
基金
辽宁省科技厅科学技术计划项目课题(2012225020)
