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

Author

Listed:
  • 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)

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.

Suggested Citation

  • Huijian Wu & Yupeng Chen & Jing Liang & Bin Shi & Ge Wu & Ying Zhang & Dan Wang & Ruifang Li & Xia Yi & Hua Zhang & Luyang Sun & Yongfeng Shang, 2005. "Hypomethylation-linked activation of PAX2 mediates tamoxifen-stimulated endometrial carcinogenesis," Nature, Nature, vol. 438(7070), pages 981-987, December.
    • Handle: RePEc:nat:nature:v:438:y:2005:i:7070:d:10.1038_nature04225
    DOI: 10.1038/nature04225
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    Cited by:

    1. Wenting Zhang & Yue Wang & Yongjie Liu & Cuifang Liu & Yizhou Wang & Lin He & Xiao Cheng & Yani Peng & Lu Xia & Xiaodi Wu & Jiajing Wu & Yu Zhang & Luyang Sun & Ping Chen & Guohong Li & Qiang Tu & Jin, 2023. "NFIB facilitates replication licensing by acting as a genome organizer," Nature Communications, Nature, vol. 14(1), pages 1-22, December.

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