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Estrogen receptor β stimulates Egr-1 transcription via MEK1/Erk/Elk-1 cascade in C6 glioma cells

  • Kim, Ji-Ha (Division of Molecular and Life Sciences, College of Science and Technology, Hanyang University) ;
  • Jeong, Il-Yeup (Division of Molecular and Life Sciences, College of Science and Technology, Hanyang University) ;
  • Lim, Yoong-Ho (Division of Bioscience and Biotechnology, BMIC) ;
  • Lee, Young-Han (Department of Biomedical Science and Technology, SMART Institute of Advanced Biomedical Science) ;
  • Shin, Soon-Young (Department of Biomedical Science and Technology, SMART Institute of Advanced Biomedical Science)
  • Received : 2011.03.11
  • Accepted : 2011.04.27
  • Published : 2011.07.31

Abstract

The Egr-1 is an immediate early response gene encoding a transcription factor that functions in the regulation of cell growth, differentiation, and apoptosis. Estrogen has diverse physiological effects, including cellular proliferation and neuroprotection against brain injury. There are two types of estrogen receptors (ERs), $ER{\alpha}$ and $ER{\beta}$. $ER{\alpha}$-induced Egr-1 expression has been extensively studied; however, the role of $ER{\beta}$ is yet not known. In the present study, we investigated whether or not $ER{\beta}$ induces Egr-1 expression in C6 rat glioma cells, which express $ER{\beta}$ but not $ER{\alpha}$. Our results show that $ER{\beta}$ promoted up-regulation of Egr-1 expression via a non-genomic mechanism involving the Raf/MEK1/Erk/Elk-1 signaling cascade.

Keywords

References

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