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Histone demethylase JMJD2B coordinates H3K4/H3K9 methylation and promotes hormonally responsive breast carcinogenesis

Lei Shi1, Luyang Sun, Qian Li

  • 1Key Laboratory of Carcinogenesis and Translational Research Ministry of Education, Department of Biochemistry and Molecular Biology, Peking University Health Science Center, Beijing 100191, China.

Proceedings of the National Academy of Sciences of the United States of America
|April 20, 2011
PubMed

Insights

The H3K9 demethylase JMJD2B coordinates with the MLL2 complex to regulate estrogen receptor activity. This epigenetic coordination is crucial for cell cycle progression and inhibits breast cancer development.

Area of Science:

  • Epigenetics
  • Molecular Biology
  • Cancer Research

Background:

  • Histone methylation at H3K4 and H3K9 are opposing epigenetic marks.
  • The coordination of these marks in mammalian cells remains unclear.

Purpose of the Study:

  • To investigate the mechanism coordinating H3K9 demethylation and H3K4 methylation.
  • To elucidate the role of JMJD2B in estrogen receptor-regulated transcription and breast cancer.

Main Methods:

  • Co-purification assays to identify protein complexes.
  • Depletion studies using siRNA to assess gene function.
  • Cell cycle analysis and in vivo tumorigenesis models.

Main Results:

  • JMJD2B, an H3K9 demethylase, is part of the MLL2 complex, a H3K4 methyltransferase.
  • The JMJD2B/MLL2 complex is required for estrogen receptor α (ERα) transcriptional activity.
  • H3K9 demethylation precedes H3K4 methylation in ERα-activated transcription.
  • JMJD2B depletion inhibits estrogen-induced cell cycle progression and breast tumor growth.
  • JMJD2B is an ERα target gene, forming a feed-forward loop.

Conclusions:

  • Establishes a molecular mechanism for coordinated H3K4 methylation and H3K9 demethylation in transcription.
  • Links JMJD2B to euchromatin regulation and breast carcinogenesis.
  • Provides insights into JMJD2B's role in hormone-responsive gene regulation and cancer.

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