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Oncogenic features of the JMJD2A histone demethylase in breast cancer

William L Berry1, Sook Shin, Stan A Lightfoot

  • 1Department of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA.

International Journal of Oncology
|September 6, 2012
PubMed

Insights

The histone demethylase JMJD2A (KDM4A) interacts with estrogen receptor alpha (ERα), promoting ERα-positive breast cancer growth. Targeting JMJD2A may offer a new therapeutic strategy for breast cancer treatment.

Area of Science:

  • Molecular biology
  • Oncology
  • Epigenetics

Background:

  • Estrogen receptor alpha (ERα) is crucial in most breast tumors.
  • Endocrine therapy is standard for ERα-positive breast cancer.
  • Mechanisms of ERα dysregulation in breast cancer are not fully understood.

Purpose of the Study:

  • To investigate the interaction between histone demethylase JMJD2A (KDM4A) and ERα.
  • To determine JMJD2A's role in ERα-mediated transcription and breast cancer cell proliferation.

Main Methods:

  • Investigated the in vivo complex formation between JMJD2A and ERα.
  • Assessed JMJD2A's coactivation of ERα-mediated transcription using wild-type and mutant forms.
  • Examined the effect of JMJD2A downregulation on cyclin D1 expression and T47D cell growth.
  • Analyzed JMJD2A expression levels in human breast tumors.

Main Results:

  • JMJD2A forms a complex with ERα in vivo.
  • Wild-type JMJD2A, but not a catalytically impaired mutant, strongly coactivates ERα-mediated transcription.
  • Downregulation of JMJD2A decreases cyclin D1 expression and reduces T47D breast cancer cell growth.
  • JMJD2A is overexpressed in human breast tumors at both mRNA and protein levels.

Conclusions:

  • JMJD2A overexpression contributes to breast tumor formation by enhancing ERα activity.
  • JMJD2A functions as a breast-relevant oncoprotein.
  • Small molecule inhibitors targeting JMJD2A's catalytic center could be valuable in breast cancer adjuvant therapy.

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