Bcl-2反义核酸增强三氧化二砷诱导NCI-H69肺癌细胞凋亡

目的 :探讨Bcl 2反义核酸对三氧化二砷 (As2 O3 )诱导NCI H6 9肺癌细胞株凋亡的影响。方法 :合成Bcl 2反义核酸 (ASON) ,导入NCI H6 9肺癌细胞。Western blot法检测Bcl 2蛋白的表达 ;FTIC TUNEL流式细胞仪检测导入ASON的NCI H6 9肺癌细胞凋亡的变化 ;Western blot法检测As2 O3 作用后多聚ADP核糖聚合酶 (PARP)裂解片段。结果 :1)导入Bcl 2反义核酸后NCI H6 9肺癌细胞 (ASON -NCI H6 9)的Bcl 2基因表达受抑制 ,Bcl 2蛋白的合成减少 ;2 )随As2 O3 浓度增加 ,肺癌细胞的凋亡指数逐渐上升 ,ASON NCI H6 9细胞凋亡指数明显高于NCI H6 9细胞 ;3)As2 O3 诱导后ASON NCI H6 9肺癌细胞PARP的89KD裂解片段检测呈强阳性 ,NCI H6 9肺癌细胞则呈弱阳性。结论 :三氧化二砷可诱导肺癌细胞株NCI H6 9凋亡 ;Bcl 2反义核酸通过阻断Bcl 2基因表达 ,增强了As2 O3 诱导NCI H6 9细胞凋亡

Bcl-2 Antisense Oligodeoxynucleotides Enhenced Apoptosis Induced by Arsenic Trioxide on Lung Cancer Cell Line NCI-H69

Objective To explore the effect of Bcl 2 antisense Oligodeoxynucleotides(ASON) to apoptosis induced by Arsenic Trioxide(As 2O 3) on lung cancer cell line NCI H69.Methods NCI H69 cell line which expresses Bcl 2 protein was treated with Bcl 2 ASON and Bcl 2 expression was detected with western blotting method.Apoptosis of cancer cells were detected by flow cytometry analysis using FTIC TUNEL(terminal deoxynucleotidyltransferase mediated dUTP nick end labelling) staining.A 89KD fragmentation of poly(ADP ribose)polymeras(PARP),which accompanied with apoptosis,was detected by Western blotting.Results Bcl 2 expression in NCI H69 cells was obviously inhibited when treated with ASON.As 2O 3 could induce apoptosis of NCI H69 cell,this effect was dose dependent.Apoptosis index in NCI H69 cells transfected with ASON was much higher than that in non transfected one.After treated with As 2O 3,89KD fragment of PARP could be detected while it was much stronger in ASON transfected ones.Conclusions Arsenic Trioxide could induce apoptosis of lung cancer cell line NCI H69.Bcl 2 ASON could enhence this effect. China J Cancer Prev Treat,2003,10(3):276-279