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

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

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。

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.