摘要
目的：探讨Ａｓ２Ｏ３对胃腺癌ＳＧＣ７９０１细胞系的生物学效应及机制。方法：通过ＭＴＴ还原法检测Ａｓ２Ｏ３对该细胞系存活率的影响，从光学显微镜形态观察，流式细胞仪分析，ＤＮＡ凝胶电泳，细胞凋亡原位检测（ＴＵＮＥＬ）进行细胞凋亡的检测。半定量ＲＴＰＣＲ检测基因表达。结果：Ａｓ２Ｏ３处理ＳＧＣ７９０１细胞后，细胞的存活率明显降低，光学显微镜下可见到明显的凋亡细胞，流式细胞仪测定细胞周期的Ｇ１期前有亚２倍体的凋亡峰，ＤＮＡ凝胶电泳显示出典型的凋亡特征：ＤＮＡ有规律断裂形成的梯状图谱，细胞凋亡原位检测发现ＤＮＡ的断裂，并降低细胞ｃｍｙｃ基因的表达。结论：Ａｓ２Ｏ３能诱导人胃腺癌ＳＧＣ７９０１细胞程序化死亡并可能通过降低ｃｍｙｃ基因的表达。
AIM: To study the biological effect of As2O3 on human gastric adenocarcinoma SGC7901 cells and its mechanisms. METHODS: MTT reduction assay, morphology investigation, flow cytometry analysis, DNA gel electrophoresis and In situ cell death detection (TUNEL), semiquantitive RTPCR were adopted. RESULTS: As2O3 inhibited the survival of SGC7901 cell line. The cells treated with As2O3 showed a typical apoptotic morphology and hypodiploid peak before G1 phase. DNA of the treated SGC7901 cells appeared a ladder pattern characteristic of apoptosis. TUNEL detection analysis also revealed DNA fragmentation. Moreover, As2O3 decreased the cmyc gene expression. CONCLUSION: As2O3 can induce programmed death of SGC7901 cells mainly via down regulation of cmyc gene expression.
出处
《药学学报》
CAS
CSCD
北大核心
1999年第5期333-337,共5页
Acta Pharmaceutica Sinica
关键词
三氧化二砷
胃腺癌
SGC7901细胞
C-MYC基因
arsenic trioxide
human gastric adenocarcinoma
SGC7901 cells
programmed cell death
cmyc gene expression
