砷剂对肺腺癌细胞凋亡及LRP、C-myc基因表达的影响

Effect and mechanism of arsenic trioxide on LRP C-myc expression in human lung adenocarcinoma cells in vitro

目的:研究三氧化二砷(arsenic trioxide,As2O3)对人肺腺癌的抑制和诱导凋亡作用及对肺耐药蛋白基因(lung resistance protein,LRP)、C-myc基因表达的影响及可能机制。方法:选用人肺腺癌A549细胞株,运用体外细胞培养法,MTT法,流式细胞术检测As2O3对人肺腺癌的抑制和诱导凋亡作用;用反转录-聚合酶链反应(RT-PCR)方法检测LRP、C-myc mRNA的表达。结果:As2O3对人肺腺癌A549细胞具有抑制作用,其抑制率呈时间-剂量依赖关系。不同浓度的As2O3均可诱导凋亡。1.0μmol/L、2.0μmol/L的As2O3可下调LRP的表达。结论:As2O3具有抑制肿瘤细胞增殖作用,主要是通过诱导细胞凋亡实现的,其机制与下调LRP、C-myc表达有密切关系。

Objective ： To study the apoptosis and mechanism of arsenic tripxide （ As2O3 ） on human lung adeno- carcinoma cells. Methods： MTT FCM and RT - PCR tests were used to investigate apoptosis levels induced by arsenic trioxide and the effect on LRP and C - myc expression. Results ： 1.0μmol/L and 2.0μmol/L arsenic trioxide can decrease LRP expression. Conclusion ： Low concentration of As2 O3 may improve apoptosis of lung cancer by decreasing LRP expression.