Phosphorylated p38 and JNK MAPK proteins in hepatocellular carcinoma

Abstract

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.