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Feedback regulation of DUSP6 transcription responding to MAPK1 via ETS2 in human cells

Toru Furukawa1, Etsuko Tanji, Shanhai Xu

  • 1International Research and Educational Institute for Integrated Medical Sciences, Tokyo Women's Medical University, Tokyo, Japan. furukawa@imcir.twmu.ac.jp

Biochemical and Biophysical Research Communications
|October 14, 2008
PubMed

Insights

The dual specificity phosphatase 6 (DUSP6) gene

Area of Science:

  • Molecular biology
  • Cellular signaling
  • Cancer research

Background:

  • Dual specificity phosphatase 6 (DUSP6/MKP-3) dephosphorylates MAPK1/ERK2, negatively regulating its activity.
  • DUSP6 expression loss in pancreatic cancer is linked to hypermethylation and constitutive MAPK1 activation.
  • Mechanisms regulating DUSP6 expression in human cells remain largely unelucidated.

Purpose of the Study:

  • To investigate the promoter activity of DUSP6 intron 1 in human cells.
  • To elucidate the role of MAPK1 activity and ETS transcription factors in DUSP6 regulation.

Main Methods:

  • Reporter assays to assess intron 1 promoter activity.
  • Analysis of ETS2 binding to the DUSP6 intron 1 promoter.
  • Correlation of promoter activity with MAPK1 activity.

Main Results:

  • DUSP6 intron 1 exhibits promoter activity in human cells.
  • Promoter activity is associated with MAPK1 activity and depends on an ETS transcription factor binding site.
  • ETS2 specifically binds to the DUSP6 intron 1 promoter.

Conclusions:

  • DUSP6 intron 1 contains functional promoter elements.
  • MAPK1 signaling, via ETS2, transcriptionally regulates DUSP6 expression through intron 1.
  • This identifies a feedback loop mechanism for DUSP6 regulation in human cells.

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