It has been demonstrated that the DcR3 gene is expressed at a low level in human embryo, lung, brain, liver, spleen, stomach, colon, lymph nodes and spinal cord, whereas it was expressed at a high level in cancers such as gastrointestinal cancer, hepatocellular carcinoma and pancreatic cancer [1
Wu et al.
] reported that the expression of DcR3 in gastric cancer patients was significantly higher than normal. DcR3 expression in the well-differentiated gastric cancer was significantly lower than that of poorly differentiated specimens (P
The DcR3 expression level was significantly associated with lymph node metastasis and pathological stage, but did not correlate with tumor size, metastatic status, or histological types. When patients were followed-up for 63
months, DcR3 overexpression was found to be associated with a significantly shortened survival rate [13
Many reports have shown that high expression levels of ERK1/2 closely correlated with breast, colorectal and pancreatic cancer, as well as malignant melanoma, leukemia and myxoma [15
Our research showed that in patients with gastric cancer, the positive incidence of DcR3 and ERK1/2 mRNA was higher than that in the non-cancerous tissues (P
0.05). RT-PCR and western blotting showed that the mRNA and protein expression levels of DcR3 and ERK1/2 in tumor tissues were significantly higher than those in non-cancer tissues, suggesting that DcR3 and ERK1/2 levels correlate with tumor development but not with age, gender or differentiation (P
Our results showed that the positive incidence of expression of DcR3 and ERK1/2 mRNA and DcR3 and ERK1/2 protein matched each other. The immunohistochemistry results also demonstrated that in gastric tumors, ERK1/2 was highly expressed.
Chen et al.
] reported that the positive rate of DcR3 expression was 74.4% (32/43) in hepatocellular carcinoma, and that there was a significant correlation between DcR3 expression and metastasis as well as recurrence and differentiation.
In the mouse gastric model, RT-PCR showed that DcR3 mRNA could be detected in tumors from day six. ERK1/2 mRNA and protein were also detected in tumors, and ERK1 levels gradually increased in gastric tumors. Furthermore, they were also detected in heart, liver, spleen, lung and kidney of the gastric cancer animal model, suggesting that they have an important role in tumor progression. ERK1/2 mRNA was detected from day four in tumor tissues, and ERK1 mRNA peaked on day 10. ERK1 protein could also be detected on day four in tumor tissues, and continued to increase every day. ERK1 remained at a stable level in heart, liver and kidney, but it decreased in lung and spleen on day 10, after reaching the peak. ERK2 was detected on day two in spleen and tumor tissues. From day four, ERK2 was detected in all six tissues, and continued to increase till day 12. ERK2 could not be detected in heart, lung and spleen by RT-PCR on day 12 in animal models, but protein levels could be detected. These results suggest that ERK1 and ERK2 might have different effects on tumor occurrence, development and clonal expansion. Many studies indicated that the expression of ERK1/2 mRNA and protein varies in different tumors and cells [20
]. Some recent reports suggested they could be entirely opposite in some cases. Thus, the effects of ERK1 and ERK2 on the tumors are unlikely to be the same.