Stress-Activated Protein Kinase/c-Jun NH2 Terminal Kinase (SAPK/JNK) Expression in Transitional Cell Carcinoma of the Urinary Bladder.
- Author:
Hyungkeun PARK
1
;
Eun Jung KIM
;
Pildu JEONG
;
Choung Soo KIM
;
Hanjong AHN
;
Wun Jae KIM
Author Information
1. Department of Urology, University of Ulsan College of Medicine, Asan Medical Ceneter, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Protein kinase;
Stress;
Bladder tumor
- MeSH:
Apoptosis;
Blotting, Western;
Carcinogenesis;
Carcinoma, Transitional Cell*;
Cell Proliferation;
Morphogenesis;
Mucous Membrane;
Phosphotransferases*;
Protein Isoforms;
Protein Kinases;
Recurrence;
Urinary Bladder Neoplasms;
Urinary Bladder*
- From:Korean Journal of Urology
2002;43(2):117-124
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: The SAPK/JNK group of MAP (mitogen-activated protein) kinases is known to regulate cellular proliferation, apoptosis and tissue morphogenesis. This study was performed to assess the clinical usefulness of the SAPK/JNK for a bladder tumor. MATERIALS AND METHODS: Ninety-five bladder tumors and 23 normal bladder mucosa were included in this study. Expression of the phosphorylated and unphosphorylated forms of JNK1 and 2 were examined using western blot analysis. The relationship between JNK expression and the bladder tumor stage, grade, recurrence, survival and P53 expression level were analyzed. RESULTS: The unphosphorylated JNK1 level was higher in bladder tumors than in normal bladder mucosa. With respect to the stage, the absolute and relative values of the phosphorylated JNK1 were higher in superficial tumors than in invasive tumors, while those of unphosphorylated JNK1 were higher in invasive tumors. The phosphorylated JNK1 level also had a negative correlation with the tumor grade and recurrence. A positive correlation existed between the p53 expression level and the absolute values of unphosphorylated JNK1 and 2. CONCLUSIONS: Among the 3 isoforms, JNK1 plays a role in the development of a bladder tumor. Higher expressions of the inactive forms in a bladder tumor than in a normal control and the active forms in a low stage and grade tumor might support the hypothesis that the loss of JNK1 activation may contribute to tumorigenesis.
