Hypomethylation-linked activation of PAX2 mediates tamoxifen-stimulated endometrial carcinogenesis

Huijian Wu, Yupeng Chen, Jing Liang, Bin Shi, Ge Wu, Ying Zhang, Dan Wang, Ruifang Li, Xia Yi, Hua Zhang, Luyang Sun and Yongfeng Shang ()
Additional contact information
Huijian Wu: Peking University Health Science Center
Yupeng Chen: Peking University Health Science Center
Jing Liang: Peking University Health Science Center
Bin Shi: Peking University Health Science Center
Ge Wu: Peking University Health Science Center
Ying Zhang: Peking University Health Science Center
Dan Wang: Peking University Health Science Center
Ruifang Li: Peking University Health Science Center
Xia Yi: Peking University Health Science Center
Hua Zhang: Peking University Health Science Center
Luyang Sun: Peking University Health Science Center
Yongfeng Shang: Peking University Health Science Center

Nature, 2005, vol. 438, issue 7070, 981-987

Abstract: Abstract Tamoxifen, a selective oestrogen receptor modulator, has been used in the treatment of all stages of hormone-responsive breast cancer. However, tamoxifen shows partial oestrogenic activity in the uterus and its use has been associated with an increased incidence of endometrial cancer. The molecular explanation for these observations is not known. Here we show that tamoxifen and oestrogen have distinct but overlapping target gene profiles. Among the overlapping target genes, we identify a paired-box gene, PAX2, that is crucially involved in cell proliferation and carcinogenesis in the endometrium. Our experiments show that PAX2 is activated by oestrogen and tamoxifen in endometrial carcinomas but not in normal endometrium, and that this activation is associated with cancer-linked hypomethylation of the PAX2 promoter.

Date: 2005
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DOI: 10.1038/nature04225

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