P53 Retards cell-growth and suppresses etoposide-induced apoptosis in Pin1-deficient mouse embryonic fibroblasts

Kiyoe Shimazaki, Takafumi Uchida, Akihiko Komine, Katsuhiko Takahashi

Research output: Contribution to journalArticlepeer-review

3 Citations (Scopus)

Abstract

We studied the effects of Pin1, a regulatory molecule of the oncosuppressor p53, on both cell cycle arrest and apoptosis by treating primary mouse embryonic fibroblasts (MEFs) with etoposide. Etoposide induced G1 arrest in both wild-type and Pin1 null (pin1 -/-) MEFs, and G2/M arrest and apoptotic cell death in MEFs lacking either p53 only (p53 -/-) or both Pin1 and p53 (pin1 -/-p53 -/-). Both pin1 -/- and pin1 -/-p53 -/- MEFs were enhanced the release of cytochrome c from the mitochondria, which might induce apoptosis. In response to etoposide treatment, apoptotic cell death was displayed in pin1 -/-p53 -/- MEFs but not in pin1 -/- MEFs. These results suggest that p53 retards growth and suppresses etoposide-induced apoptosis in pin1 -/- MEFs.

Original languageEnglish
Pages (from-to)133-138
Number of pages6
JournalBiochemical and biophysical research communications
Volume422
Issue number1
DOIs
Publication statusPublished - 2012 May 25

Keywords

  • Apoptosis
  • Etoposide
  • Mitochondria
  • P53
  • Pin1

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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