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Interleukin-1 receptor antagonist mRNA expression and the progression of gastric carcinoma

Interleukin-1 receptor antagonist (IL-1ra), an endogeneous inhibitor of IL-1, plays an immunosuppressive role in vivo by blocking the proinflammatory effects of IL-1. In the present study, we examined whether IL-1ra expression in human gastric carcinoma correlates with tumor progression and/or metas...

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Published in:Cancer letters 1999-08, Vol.142 (2), p.179-184
Main Authors: Iizuka, Norio, Hazama, Shoichi, Hirose, Kunitaka, Abe, Tosihiro, Tokuda, Nobuko, Fukumoto, Tetsuo, Tangoku, Akira, Oka, Masaaki
Format: Article
Language:English
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Summary:Interleukin-1 receptor antagonist (IL-1ra), an endogeneous inhibitor of IL-1, plays an immunosuppressive role in vivo by blocking the proinflammatory effects of IL-1. In the present study, we examined whether IL-1ra expression in human gastric carcinoma correlates with tumor progression and/or metastatic potential. The reverse transcription-polymerase chain reaction was used to compare the expression of the secreted form of IL-1ra (sIL-1ra) and the intracellular form of IL-1ra (icIL-1ra) mRNA in tumor and corresponding benign tissue obtained from 38 patients with gastric carcinoma. The incidence of sIL-1ra mRNA expression was significantly higher in tumor (52%) than in corresponding benign tissue (18%) ( P=0.002). On the contrary, icIL-1ra mRNA was detected in all tumors and benign tissues. The expression of sIL-1ra mRNA by malignant tissue correlated positively with both lymph node metastasis ( P=0.008) and liver metastasis ( P=0.015). There was no association between tumor sIL-1ra mRNA expression and other clinicopathologic factors. The degree of regional lymph node reaction, such as sinus histiocytosis, in tumors expressing sIL-1ra mRNA was significantly weaker than that in tumors without sIL-1ra mRNA expression (5/20 vs. 12/18, P=0.010). These results demonstrate that the altered expression of sIL-1ra by malignant tissue may be related to the progression of gastric carcinoma via modulating host immune response.
ISSN:0304-3835
1872-7980
DOI:10.1016/S0304-3835(99)00162-7