Estrogen regulates DNA methyltransferase 3B expression in Ishikawa endometrial adenocarcinoma cells
Estrogen regulates DNA methyltransferase 3B expression in Ishikawa endometrial adenocarcinoma cells
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DOI：
10.1007/s11033-008-9435-9
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发表时间：
2009-11-01
影响因子：
2.8
通讯作者：
Wang, Fei
中科院分区：
文献类型：
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作者：
Cui, Min;Wen, Zeqing;Wang, Fei
众所周知，暴露于无对抗性雌激素被认为是子宫内膜癌的一个重要危险因素。最近的研究表明，DNA甲基转移酶（dnmt）的过表达参与了子宫内膜癌的发展。因此，本研究旨在阐明雌激素对子宫内膜癌中dnmt表达的影响。采用石川细胞系。流式细胞术分析显示，17 β -雌二醇（E-2）促进细胞增殖，在10(-8)m时达到峰值，实时荧光定量PCR和western blotting分析证实E-2处理后DNMT3B过表达。此外，添加ICI182780可抑制E-2诱导的DNMT3B表达上调。然而，我们没有观察到DNMT1表达的变化。我们的研究提示雌激素通过er依赖途径上调DNMT3B的表达可能是雌激素促进子宫内膜癌细胞恶性转化的可能机制。
It is well-known that exposure to unopposed estrogen is considered as an important risk factor for endometrial cancer. Recent studies have shown that over-expression of DNA methyltransferases (DNMTs) are involved in the development of endometrial cancer. Therefore, the present study was undertaken to elucidate the impact of estrogen on the expression of DNMTs in endometrial cancer. Ishikawa cell line was used. Flow cytometry analysis demonstrated that 17 beta-estradiol (E-2) enhanced the cell proliferation with a peak at 10(-8) M. Over-expression of DNMT3B treated with E-2 was confirmed by real-time PCR and western blotting analysis. Furthermore, the up-regulation of DNMT3B expression induced by E-2 was suppressed by the addition of ICI182780. However, we did not observe changes in the expression of DNMT1. Our study suggests that estrogen up-regulating the expression of DNMT3B in an ER-dependent pathway may be a possible mechanism for estrogen facilitates the malignant transformation of endometrial cancer cells.