摘要
目的探讨三氧化二砷促进未分化甲状腺癌FRO细胞凋亡的机制,为临床治疗提供参考。方法将生长状态良好的未分化甲状腺癌FRO细胞随机分为5组:对照组、U0126(10μM)组、三氧化二砷低剂量(1μM)组、三氧化二砷中剂量(10μM)组、三氧化二砷高剂量(100μM)组。分析各组细胞凋亡蛋白、ERK通路蛋白表达。结果研究发现三氧化二砷能引起未分化甲状腺癌FRO细胞Bax、Caspase-3和Caspase-6蛋白表达增强以及Raf、Ras、MEK、ERK1/2和Bcl-2表达减弱(P﹤0.05),且高剂量效果比中剂量和低剂量更显著(P﹤0.05)。结论三氧化二砷能有效促进未分化甲状腺癌FRO细胞凋亡,且此过程与其抑制ERK信号转导通路蛋白过表达有关。
Objective To explore the mechanism of As2O3 in regulating the apoptosis of anaplastic thyroid cancer（ATC） cell line FRO. Method Cultivated ATC cell line FRO were randomized into 5 groups, as control group, U0126group（10 μM）, low level As2O3group（1 μM）, moderate level As2O3group（10 μM） and high level As2O3group（100μM）. The expression of apoptotic proteins and ERK signaling transduction proteins were assayed by ELISA. Result The expression of Bax, Caspase-3 and Caspase-6 proteins were significantly increased（P〈0.05）, while the expression of Bcl2,Ras, Raf MEK and ERK1/2 proteins were decreased（P〈0.05） with the treatment of As2O3, and the effects were positively correlated with dose levels（P〈0.05）. Conclusion As2O3 may significantly promote the apoptosis of anaplastic thyroid cancer cell line FRO, which is possibly correlated with the inhibited overexpression of ERK signaling pathway.
出处
《癌症进展》
2016年第9期879-881,共3页
Oncology Progress
