Phosphorylated p38 and JNK MAPK proteins in hepatocellular carcinoma
Article first published online: 3 OCT 2012
© 2012 The Authors. European Journal of Clinical Investigation © 2012 Stichting European Society for Clinical Investigation Journal Foundation
European Journal of Clinical Investigation
Volume 42, Issue 12, pages 1295–1301, December 2012
How to Cite
Wang, S.-N., Lee, K.-T., Tsai, C.-J., Chen, Y.-J. and Yeh, Y.-T. (2012), Phosphorylated p38 and JNK MAPK proteins in hepatocellular carcinoma. European Journal of Clinical Investigation, 42: 1295–1301. doi: 10.1111/eci.12003
- Issue published online: 20 NOV 2012
- Article first published online: 3 OCT 2012
- Accepted manuscript online: 14 SEP 2012 04:29AM EST
- Received 7 March 2012; accepted 29 August 2012
- Jun N-terminal kinase;
- hepatocellular carcinoma
Eur J Clin Invest 2012; 42 (12): 1295–1301
Background The p38 and JNK MAPK proteins function as key mediators in cellular responses to extracellular stimuli. Deregulated p38 and JNK expressions have been associated with cancer development. This study aimed to investigate the association of p-p38 and p-JNK levels of the cancerous tissues with hepatocellular carcinoma (HCC) development.
Materials and methods One hundred and four liver cancer tissues of patients with HCC who underwent curative resection were prospectively collected. The levels of activated/p-p38 and p-JNK were determined by the enzyme-linked immunosorbent assay. The associations of results with clinicopathological characteristics and overall survival were further statically analysed using chi-squared test, two-tailed Student’s t-test and Kaplan–Meier survival curve.
Results The p-p38 levels were significantly higher in the HCC patients with a larger tumour (≥ 3 cm) and satellite tumour, and significantly correlated with the p-JNK levels. High p-p38 and low p-JNK expressions were associated with a poor survival in the patients with HCC (odds ratio, 4·24 and 0·20; P = 0·03 and 0·03, respectively). The Kaplan–Meier survival analysis showed that the HCC patients with high p-p38 expressions had a poor overall survival than those with low p-p38 expressions (P = 0·04), and a coexistent and high p-JNK expression remarkably improved this trend.
Conclusions Increasing p-p38 levels in HCC tissues were associated with tumour size and the formation of satellite tumours. High p-p38 expression could serve as a predictor for a poor survival for the patients with HCC. Simultaneous expression of p-JNK in HCC tissues might antagonize the promoting effect of p-p38 in human liver cancer.