诱导型一氧化氮合酶与环氧合酶-2在肿瘤组织中的共表达

诱导型一氧化氮合酶(iNOS)和环氧合酶-2(COX-2)均与肿瘤发生、生长、血管形成及转移有关。在正常生理条件下，两者在多数组织内均检测不到，但在受到各种病理因素的刺激后，两者均能被迅速诱导表达。在许多恶性肿瘤组织中，两者的表达一致上调，呈正相关，其联合表达与肿瘤的生物学行为密切相关。研究发现iNOS与COX-2有可能通过Wnt-β-catenin信号实现了信息交流和相互调控，并通过这种机制，共同在肿瘤的各种生物学行为中发挥作用。

Co-expression of inducible nitric oxide synthase andcyclooxygenase-2 in carcinoma tissue

Inducible nitric oxide synthase(iNOS) and cyclooxygenase-2 (COX-2) play important roles in carcinogenesis,growth,invasion, and metastasis. They are undetectable in most normal tissues but highly inducible by inflammatory cytokines, tumor promoters, growthtactors,and so on. COX-2 overexpression has been detected in various malignancies. The mechanisms that underlie the tumorigenic effect of COX-2 include the inhibition of apoptosis, the increase of metastatic potential, tumor angiogenesis and inhibited immunity.Co-overexpressions of iNOS and COX-2 were detected in various malignancies,e.g,colorectal cancer,breast cancer,endometrial carcinoma,astrocytic gliomas, head and neck squamous cell carcinoma. iNOS expression is significantly associated with COX-2 expression. There was a positive relationship between iNOS and COX-2. However, one study showed that the overexpression of COX-2 had nothing to do with iNOS in nasopharyngeal carcinoma(NPC) tissues. There is cross-talk between iNOS and COX-2.It is suggested that the signal pathway of cytokine-induced iNOS and COX-2 coexpression is tightly associated. However, the exact cellular mechanism of NO in PGE2 formation and the relationship between NO and COX-2 and the co-overexpressions of iNOS and COX-2 how to result in carcinogenesis,growth,invasion,metastasis are not clear. Accoding to the existed studies, the cross-talk and the mechanisms in carcinoma between iNOS and COX-2 maybe practice by the canonical Wnt-β-catenin signaling pathway. iNOS and COX-2 may become new anticancer targets if the further study were done and these mechanisms were maken clear.