Background: Cyclooxygenase is the only rate-limiting enzymeof prostaglandin. By far two subtypes were found. There are COX-1and COX-2. In recent years some studies found that COX-2 plays animportant role in the cancinogenesis, development and prognosis.Based on this, some scientists investigated that COX-2 inhibitorshave anti-tumor effect. Generally COX-1 and COX-2 can beexamined in human tissues. The former is expressed constitutively,and the later is expressed induciblely. Physically COX-2 mRNA andprotein are few, and COX-2 mRNA can be examined. However,COX-2 protein can not be examined, but it is important inmaintaining the normal physical functions of many organs andtissues. In pathological condition, such as inflammation and cancer,COX-2 mRNA and protein expressions are upregulated.Many researchers investigated COX-2 expression in tumors,and the difference has statistical significance compared with itsexpression in normal tissues. In some benign neoplasms COX-2expression can be examined, such as adenomas. COX-2 can induceneoplasms by many pathways, such as inhibiting tumor cellapoptosis, promoting angiogenesis, inhibiting immune function andincreasing tumor metastasis. However, the definite mechanism is stillunclear.Generally the growth of tumor is dependent on rich blood tosupply enough nutrition and oxygen. Therefore, the ability to induceangiogenesis is very important for the growth of tumors. Vascularendothelial growth factor (VEGF) is the strong factor to induceangiogenesis. So we infer that COX-2 may by inducing VEGFexpression promote carcinogenesis.Objective: Cyclooxygenase (COX-2) is one of the rate-limitingenzymes in metabolism of arachidonic acid, and COX-2 inhibitorshave potential preventive effects of cancer. The underlyingmechanism is unclear. The aim of this study was to investigate theexpression of COX-2 and VEGF in thyroid neoplasms and itsclinical significance.Materials and Methods: Immunohistochemistry was used todetect the expression of COX-2 and VEGF in 60 thyroid cancer and15 thyroid adenomas. Reverse transcriptase PCR (RT-PCR) was usedto examine the COX-2 mRNA and VEGF mRNA expressions in 15thyroid cancers and 15 thyroid adenomas.Results: The expression rate of COX-2 and VEGF in thyroidcancers were higher than those in thyroid adenomas (P<0.01). Theexpression of COX-2 and VEGF in thyroid cancer presented positivecorrelation (r=0.636, P<0.01). The expression rate of COX-2 inthyroid papillary cancer and undifferentiated cancer were 47.1% and90.0%(P<0.05).The expression rate of VEGF in thyroid papillarycancer and undifferentiated cancer were 71.4%and 100%(P<0.05).The expression rate of COX-2 and VEGF in TNM I and II werelower than those in TNM III and IV (P<0.05). The expression rate ofthyroid cancer with lymphatic metastasis was higher than thatwithout lymphatic metastasis (P<0.05). The result was furtherverified by the results of RT-PCR.Conclusions: COX-2 and VEGF contributes to thyroid cancer.The expression of COX-2 and VEGF in thyroid cancer correlateswith pathological type, TNM phase and lymphatic metastasis.COX-2 may potentially regulate the expression of VEGF, thenpromots the infiltration and metastasis of thyroid cancer. Theover-expression of COX-2 may be an early event of thyroidneoplasms. It may work as a molecule marker of thyroid cancer forearly diagnosis, and as a target of drug treatment for thyroid cancer.Because COX-2 is relevant to cancinogenesis, it maypotentially work as an effective target of tumor genetic therapy andbiological therapy. The application of COX-2 inhibitor to treattumors is one of focuses of tumor research. And many studies haveconfirmed that COX-2 inhibitor has anti-tumor effect. COX-2inhibitor is well-known non-steroid anti-inflammatory drugs(NSAIDs), such as prostaglandin (PG). As mentioned above,NSAIDs can promote tumor cell apoptosis and inhibit angiogenesisby inhibiting COX-2 expression. So it can not only be used in tumorchemo-prevention, but in clinical therapy. In the future the focus is todiscuss the proper dosage, time point and safety of NSAIDs to treattumors. In this way a reliable plan is available for tumor preventionand anti-cancer therapy. |