Involvement of JNK-initiated p53 accumulation and phosphorylation of p53 in pseudolaric acid B induced cell death.
- Author:
Xianfeng GONG
1
;
Minwei WANG
;
Shin ichi TASHIRO
;
Satoshi ONODERA
;
Takashi IKEJIMA
Author Information
1. China-Japan Research Institute of Medical and Pharmaceutical Sciences, Shenyang Pharmaceutical University, Shenyang 110016, China. ikejimat@vip.sina.com
- Publication Type:Original Article
- Keywords:
apoptosis;
HeLa cells;
JNK mitogen-activated protein kinases;
protein kinase C;
pseudolaric acid B;
tumor suppressor protein p53
- MeSH:
Tumor Suppressor Protein p53/metabolism/*physiology;
Protein Kinase C/metabolism;
Phosphorylation;
JNK Mitogen-Activated Protein Kinases/*physiology;
Humans;
Hela Cells;
Diterpenes/*pharmacology;
DNA Fragmentation/drug effects;
Cell Death/*drug effects;
Anthracenes/pharmacology
- From:Experimental & Molecular Medicine
2006;38(4):428-434
- CountryRepublic of Korea
- Language:English
-
Abstract:
A terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assay was used to determine that apoptosis causes HeLa cell death induced by pseudolaric acid B. The c-Jun N-terminal kinase (JNK) inhibitor SP600125 decreased p53 protein expression during exposure to pseudolaric acid B. SP600125 decreased the phosphorylation of p53 during pseudolaric acid B exposure, indicating that JNK mediates phosphorylation of p53 during the response to pseudolaric acid B. SP600125 reversed pseudolaric acid B-induced down-regulation of phosphorylated extracellular signal-regulated protein kinase (ERK), and protein kinase C (PKC) was activated by pseudolaric acid B, whereas staurosporine, calphostin C, and H7 partly blocked this effect. These results indicate that p53 is partially regulated by JNK in pseudolaric acid B-induced HeLa cell death and that PKC participates in pseudolaric acid B-induced HeLa cell death.
