Estrogen regulates DNA methyltransferase 3B expression in Ishikawa endometrial adenocarcinoma cells

被引：35

作者：

Cui, Min ^{[1
]}

Wen, Zeqing ^{[1
]}

Yang, Zhongli ^{[1
]}

Chen, Ji ^{[2
]}

Wang, Fei ^{[1
]}

机构：

[1] Shandong Univ, Shandong Prov Hosp, Dept Obstet & Gynecol, Jinan 250021, Shandong, Peoples R China

[2] Shandong Univ, Shandong Prov Hosp, Dept Urol, Jinan 250021, Shandong, Peoples R China

来源：

MOLECULAR BIOLOGY REPORTS | 2009年 / 36卷 / 08期

关键词：

Endometrial cancer; Carcinogenesis; Estrogen; Estrogen receptor; DNA methyltransferase; PROMOTER METHYLATION; MISMATCH REPAIR; HUMAN CANCER; GENE; CARCINOMA; HYPERMETHYLATION; TUMORIGENESIS; PHENOTYPE; RECEPTOR;

D O I：

10.1007/s11033-008-9435-9

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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.

引用

页码：2201 / 2207

页数：7

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