[三氧化二砷诱导骨髓增生异常综合征细胞系MUTZ-1中p15INK4B基因表达]
[Arsenic trioxide induced p15INK4B gene expression in myelodysplastic syndrome cell line MUTZ-1].
作者信息
Tong Hongyan, Lin Maofang
机构信息
The First Affiliated Hospital, Medical College of Zhejiang University, Hangzhou 310003, China.
出版信息
Zhonghua Xue Ye Xue Za Zhi. 2002 Dec;23(12):638-41.
OBJECTIVE
To investigate the mechanisms of arsenic trioxide (As(2)O(3)) induced demethylation.
METHOD
Methylation of p15INK4B gene in MUTZ-1 cell was detected by PCR using a methylation specific primer (MSP), the expression of P15, DNA methyltransferase (DNMT) 1, DNMT3A and DNMT3B gene by RT-PCR, the As(2)O(3) induced growth inhibition of MUTZ-1 cell by MTT method.
RESULTS
P15 gene failed to express in MUTZ-1 cells after methylation. The expression was recovered after the cells exposed to As(2)O(3). As(2)O(3) could significantly down-regulate DNMT3A and DNMT3B but not DNMT1 gene on mRNA level in a dose dependent manner.
CONCLUSION
As(2)O(3) could activate the expression of p15 gene by demethylation or/and by inhibiting DNMT3A and DNMT3B gene.
目的
研究三氧化二砷（As₂O₃）诱导去甲基化的机制。
方法
采用甲基化特异性引物（MSP）通过PCR检测MUTZ-1细胞中p15INK4B基因的甲基化情况，采用RT-PCR检测P15、DNA甲基转移酶（DNMT）1、DNMT3A和DNMT3B基因的表达，采用MTT法检测As₂O₃对MUTZ-1细胞生长的抑制作用。
结果
甲基化后MUTZ-1细胞中P15基因未表达。细胞暴露于As₂O₃后表达恢复。As₂O₃可在mRNA水平以剂量依赖方式显著下调DNMT3A和DNMT3B基因，但对DNMT1基因无影响。
结论
As₂O₃可通过去甲基化或/和抑制DNMT3A和DNMT3B基因激活p15基因的表达。
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