TY - JOUR
T1 - P53 Retards cell-growth and suppresses etoposide-induced apoptosis in Pin1-deficient mouse embryonic fibroblasts
AU - Shimazaki, Kiyoe
AU - Uchida, Takafumi
AU - Komine, Akihiko
AU - Takahashi, Katsuhiko
N1 - Funding Information:
We acknowledge A Kondo, Y Bamba, N Takahashi, D Sato, K Ikeda, T Hasegawa, N H Choi-Miura and M Tomita for their technical help. This work was supported in part by Grant-in-Aid for Scientific Research on Priority Areas, Grant-in-Aid for Scientific Research, Special Research Grant-in Aid for Development of Characteristic Education from the Ministry of Education, Culture, Sports, Science and Technology of Japan (TU) , Center for Interdisciplinary Research Tohoku University for Specially Promoted Research (TU) , Showa University Grant-in Aid for Innovative Collaborative Research Projects and the Open Research Center Project (KT).
PY - 2012/5/25
Y1 - 2012/5/25
N2 - 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.
AB - 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.
KW - Apoptosis
KW - Etoposide
KW - Mitochondria
KW - P53
KW - Pin1
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U2 - 10.1016/j.bbrc.2012.04.121
DO - 10.1016/j.bbrc.2012.04.121
M3 - Article
C2 - 22564744
AN - SCOPUS:84861459486
SN - 0006-291X
VL - 422
SP - 133
EP - 138
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 1
ER -