Knockdown of p53 suppresses Nanog expression in embryonic stem cells

Essam Mohamed, Ikuo Tooyama

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

Mouse embryonic stem cells (ESCs) express high levels of cytoplasmic p53. Exposure of mouse ESCs to DNA damage leads to activation of p53, inducing Nanog suppression. In contrast to earlier studies, we recently reported that chemical inhibition of p53 suppresses ESC proliferation. Here, we confirm that p53 signaling is involved in the maintenance of mouse ESC self-renewal. RNA interference-mediated knockdown of p53 induced downregulation of p21 and defects in ESC proliferation. Furthermore, p53 knockdown resulted in a significant downregulation in Nanog expression at 24 and 48 h post-transfection. p53 knockdown also caused a reduction in Oct4 expression at 48 h post-transfection. Conversely, exposure of ESCs to DNA damage caused a higher reduction of Nanog expression in control siRNA-treated cells than in p53 siRNA-treated cells. These data show that in the absence of DNA damage, p53 is required for the maintenance of mouse ESC self-renewal by regulating Nanog expression.

Original languageEnglish
Pages (from-to)652-657
Number of pages6
JournalBiochemical and Biophysical Research Communications
Volume443
Issue number2
DOIs
Publication statusPublished - 10 Jan 2014

Fingerprint

Embryonic Stem Cells
Stem cells
DNA Damage
Small Interfering RNA
Transfection
Down-Regulation
Maintenance
Cell Proliferation
Cell proliferation
RNA Interference
DNA
Cells
Mouse Embryonic Stem Cells
Chemical activation
RNA
Defects
Cell Self Renewal

Keywords

  • DNA damage
  • ESCs
  • Knockdown
  • Oct4
  • Self-renewal
  • Tumor suppressor gene

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

Cite this

Knockdown of p53 suppresses Nanog expression in embryonic stem cells. / Mohamed, Essam; Tooyama, Ikuo.

In: Biochemical and Biophysical Research Communications, Vol. 443, No. 2, 10.01.2014, p. 652-657.

Research output: Contribution to journalArticle

@article{d463ab324aac44c99df8f3305f966a53,
title = "Knockdown of p53 suppresses Nanog expression in embryonic stem cells",
abstract = "Mouse embryonic stem cells (ESCs) express high levels of cytoplasmic p53. Exposure of mouse ESCs to DNA damage leads to activation of p53, inducing Nanog suppression. In contrast to earlier studies, we recently reported that chemical inhibition of p53 suppresses ESC proliferation. Here, we confirm that p53 signaling is involved in the maintenance of mouse ESC self-renewal. RNA interference-mediated knockdown of p53 induced downregulation of p21 and defects in ESC proliferation. Furthermore, p53 knockdown resulted in a significant downregulation in Nanog expression at 24 and 48 h post-transfection. p53 knockdown also caused a reduction in Oct4 expression at 48 h post-transfection. Conversely, exposure of ESCs to DNA damage caused a higher reduction of Nanog expression in control siRNA-treated cells than in p53 siRNA-treated cells. These data show that in the absence of DNA damage, p53 is required for the maintenance of mouse ESC self-renewal by regulating Nanog expression.",
keywords = "DNA damage, ESCs, Knockdown, Oct4, Self-renewal, Tumor suppressor gene",
author = "Essam Mohamed and Ikuo Tooyama",
year = "2014",
month = "1",
day = "10",
doi = "10.1016/j.bbrc.2013.12.030",
language = "English",
volume = "443",
pages = "652--657",
journal = "Biochemical and Biophysical Research Communications",
issn = "0006-291X",
publisher = "Academic Press Inc.",
number = "2",

}

TY - JOUR

T1 - Knockdown of p53 suppresses Nanog expression in embryonic stem cells

AU - Mohamed, Essam

AU - Tooyama, Ikuo

PY - 2014/1/10

Y1 - 2014/1/10

N2 - Mouse embryonic stem cells (ESCs) express high levels of cytoplasmic p53. Exposure of mouse ESCs to DNA damage leads to activation of p53, inducing Nanog suppression. In contrast to earlier studies, we recently reported that chemical inhibition of p53 suppresses ESC proliferation. Here, we confirm that p53 signaling is involved in the maintenance of mouse ESC self-renewal. RNA interference-mediated knockdown of p53 induced downregulation of p21 and defects in ESC proliferation. Furthermore, p53 knockdown resulted in a significant downregulation in Nanog expression at 24 and 48 h post-transfection. p53 knockdown also caused a reduction in Oct4 expression at 48 h post-transfection. Conversely, exposure of ESCs to DNA damage caused a higher reduction of Nanog expression in control siRNA-treated cells than in p53 siRNA-treated cells. These data show that in the absence of DNA damage, p53 is required for the maintenance of mouse ESC self-renewal by regulating Nanog expression.

AB - Mouse embryonic stem cells (ESCs) express high levels of cytoplasmic p53. Exposure of mouse ESCs to DNA damage leads to activation of p53, inducing Nanog suppression. In contrast to earlier studies, we recently reported that chemical inhibition of p53 suppresses ESC proliferation. Here, we confirm that p53 signaling is involved in the maintenance of mouse ESC self-renewal. RNA interference-mediated knockdown of p53 induced downregulation of p21 and defects in ESC proliferation. Furthermore, p53 knockdown resulted in a significant downregulation in Nanog expression at 24 and 48 h post-transfection. p53 knockdown also caused a reduction in Oct4 expression at 48 h post-transfection. Conversely, exposure of ESCs to DNA damage caused a higher reduction of Nanog expression in control siRNA-treated cells than in p53 siRNA-treated cells. These data show that in the absence of DNA damage, p53 is required for the maintenance of mouse ESC self-renewal by regulating Nanog expression.

KW - DNA damage

KW - ESCs

KW - Knockdown

KW - Oct4

KW - Self-renewal

KW - Tumor suppressor gene

UR - http://www.scopus.com/inward/record.url?scp=84892432931&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84892432931&partnerID=8YFLogxK

U2 - 10.1016/j.bbrc.2013.12.030

DO - 10.1016/j.bbrc.2013.12.030

M3 - Article

VL - 443

SP - 652

EP - 657

JO - Biochemical and Biophysical Research Communications

JF - Biochemical and Biophysical Research Communications

SN - 0006-291X

IS - 2

ER -