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Dux4 induces cell cycle arrest at G1 phase through upregulation of p21 expression

Hongliang Xu1, Zhaoxia Wang1, Suqin Jin1

  • 1Department of Neurology, Peking University First Hospital, Beijing 100034, China.

Biochemical and Biophysical Research Communications
|March 5, 2014
PubMed

Insights

Facioscapulohumeral dystrophy involves DUX4 retrogene. Overexpressing DUX4 inhibits cell proliferation by increasing p21, a cell cycle regulator, via Sp1 transcription factor activation.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cell Biology

Background:

  • Facioscapulohumeral dystrophy (FSHD) is linked to DUX4 retrogene activity.
  • The precise mechanisms of DUX4-induced myopathy remain unclear.

Purpose of the Study:

  • To investigate the impact of DUX4 overexpression on cell proliferation and cell cycle progression.
  • To elucidate the downstream molecular events regulated by DUX4, focusing on the p53/p21 signaling pathway.

Main Methods:

  • TE671 cell model for DUX4 overexpression.
  • Analysis of cell proliferation, cell cycle phase distribution (G1 arrest).
  • Western blotting, qRT-PCR for p53, phospho-p53, and p21.
  • p21 promoter activity assays, Sp1 expression analysis.
  • Chromatin immunoprecipitation (ChIP) assays.

Main Results:

  • DUX4 overexpression reduced cell proliferation and caused G1 phase arrest.
  • p21 mRNA and protein levels were significantly increased by DUX4, while p53 levels remained unchanged.
  • Silencing p21 expression rescued the proliferation defect and cell cycle arrest induced by DUX4.
  • DUX4 enhanced p21 promoter activity, which was dependent on Sp1 transcription factor binding.
  • ChIP assays confirmed DUX4-induced Sp1 binding to the p21 promoter in vivo.

Conclusions:

  • DUX4 induces cell proliferation inhibition and G1 phase arrest.
  • This effect is mediated through the upregulation of p21.
  • Sp1 transcription factor plays a critical role in DUX4-induced p21 expression.
Keywords:
Cell cycleDux4FSHDp21

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