Exp Mol Med.  2006 Aug;38(4):428-434.

Involvement of JNK-initiated p53 accumulation and phosphorylation of p53 in pseudolaric acid B induced cell death

Affiliations
  • 1China-Japan Research Institute of Medical and Pharmaceutical Sciences, Shenyang Pharmaceutical University, Shenyang 110016, China. ikejimat@vip.sina.com
  • 2Department of Pharmacology, Shenyang Pharmaceutical University, Shenyang 110016, China.
  • 3Department of Clinical and Biomedical Sciences, Showa Pharmaceutical University, Tokyo 194-8543, Japan.

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.

Keyword

apoptosis; HeLa cells; JNK mitogen-activated protein kinases; protein kinase C; pseudolaric acid B; tumor suppressor protein p53

MeSH Terms

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
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