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.
|Number of pages||6|
|Journal||Biochemical and biophysical research communications|
|Publication status||Published - 2012 May 25|
ASJC Scopus subject areas
- Molecular Biology
- Cell Biology