【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。更多还原

【Abstract】 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.更多还原