重庆医学
重慶醫學
중경의학
CHONGQING MEDICAL JOURNAL
2015年
24期
3325-3327
,共3页
甲状腺肿瘤%细胞增殖%cAMP%dbcAMP%Raf1
甲狀腺腫瘤%細胞增殖%cAMP%dbcAMP%Raf1
갑상선종류%세포증식%cAMP%dbcAMP%Raf1
thyroid neoplasms%cell proliferation%cyclic AMP%dbcAMP%Raf1
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。
目的:探討雙丁酰環腺苷痠(dbcAMP)對甲狀腺癌細胞株 FTC-133增殖的影響。方法將 FTC-133細胞進行常規培養,分為對照組,處理組(dbcAMP 0.5、1.0、2.0 mmol/L)共4組。採用四甲基偶氮唑藍(MTT)法、生長麯線法觀察0.5、1.0、2.0 mmol/L dbcAMP 經24 h、48 h 對甲狀腺癌細胞株 FTC-133細胞增殖能力的影響,流式細胞術檢測細胞週期的變化情況,使用反轉錄定量 PCR(RT-qPCR)和蛋白免疫印跡實驗(Western Blotting)方法檢測 Raf1的 mRNA 和蛋白錶達水平。結果與對照組比較,不同濃度 dbcAMP 和時間處理的 FTC-133細胞增殖均受抑製,併錶現齣時間-劑量依賴性;S 期細胞顯著減少,G2/M期細胞顯著增加;Raf1 mRNA 和蛋白水平明顯減低。結論dbcAMP 顯著降低甲狀腺癌細胞株 FTC-133的增殖能力,促進凋亡,可能與激活 ERK MAPK 通路有關。
목적:탐토쌍정선배선감산(dbcAMP)대갑상선암세포주 FTC-133증식적영향。방법장 FTC-133세포진행상규배양,분위대조조,처리조(dbcAMP 0.5、1.0、2.0 mmol/L)공4조。채용사갑기우담서람(MTT)법、생장곡선법관찰0.5、1.0、2.0 mmol/L dbcAMP 경24 h、48 h 대갑상선암세포주 FTC-133세포증식능력적영향,류식세포술검측세포주기적변화정황,사용반전록정량 PCR(RT-qPCR)화단백면역인적실험(Western Blotting)방법검측 Raf1적 mRNA 화단백표체수평。결과여대조조비교,불동농도 dbcAMP 화시간처리적 FTC-133세포증식균수억제,병표현출시간-제량의뢰성;S 기세포현저감소,G2/M기세포현저증가;Raf1 mRNA 화단백수평명현감저。결론dbcAMP 현저강저갑상선암세포주 FTC-133적증식능력,촉진조망,가능여격활 ERK MAPK 통로유관。
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.