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Knockdown of p53 suppresses Nanog expression in embryonic stem cells

Essam Mohamed Abdelalim1, Ikuo Tooyama2

  • 1Qatar Biomedical Research Institute, Qatar Foundation, Doha 5825, Qatar; Molecular Neuroscience Research Center, Shiga University of Medical Science, Setatsukinowa-cho, Otsu, Shiga 520-2192, Japan; Department of Cytology and Histology, Faculty of Veterinary Medicine, Suez Canal University, Ismailia, Egypt.

Biochemical and Biophysical Research Communications
|December 17, 2013
PubMed

Insights

p53 protein is crucial for maintaining mouse embryonic stem cell (ESC) self-renewal. Suppressing p53 disrupts ESC proliferation and downregulates key stem cell markers like Nanog and Oct4.

Area of Science:

  • Stem Cell Biology
  • Molecular Biology
  • Cell Signaling

Background:

  • Mouse embryonic stem cells (ESCs) express high levels of cytoplasmic p53.
  • DNA damage in ESCs activates p53, leading to Nanog suppression.
  • Previous studies indicated p53 inhibition affects ESC proliferation.

Purpose of the Study:

  • To confirm the role of p53 signaling in maintaining mouse ESC self-renewal.
  • To investigate the effect of p53 knockdown on ESC proliferation and key stem cell markers.

Main Methods:

  • RNA interference (RNAi)-mediated knockdown of p53 in mouse ESCs.
  • Analysis of p21, Nanog, and Oct4 expression levels post-transfection.
  • Assessment of ESC proliferation defects.

Main Results:

  • p53 knockdown led to downregulation of p21 and impaired ESC proliferation.
  • Significant reduction in Nanog expression at 24 and 48 hours post-p53 knockdown.
  • Oct4 expression was reduced at 48 hours post-p53 knockdown.
  • DNA damage caused greater Nanog reduction in control cells compared to p53-depleted cells.

Conclusions:

  • p53 signaling is essential for the self-renewal of mouse ESCs.
  • In the absence of DNA damage, p53 regulates Nanog expression to maintain ESC self-renewal.
Keywords:
DNA damageESCsKnockdownOct4Self-renewalTumor suppressor gene

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