| Objective: Malignant tumor in a serious threat to human health and life, about 700 million people worldwide each year died of cancer. While colorectal cancer is one of common malignant tumor of digestive tract -- the number of CRC patients increases by 2% each year, which aroused global concern.Studies have shown that colorectal cancer was the results of colon epithelial cells affected by both genetic and environmental factors such as the role of genetic aberrations leading to. To date, the exact pathogenesis of colorectal cancer is still not very clear, but with the development and extensive application of molecular biology techniques, the characteristic of the molecular genetics of colorectal cancer has been gradually understood. Currently, generally agreed that colorectal cancer is a matter of multi-gene, multi-step complex process involving multiple oncogene activation and tumor suppressor gene inactivation.Cyclooxygenas (COX) also known as the peroxidase of cyclooxygenase prostaglandin synthesis enzyme, it is an important rate-limiting enzyme for prostaglandin's synthesis, and it can decompose arachidonic acid into variety of prostaglandin products, thus it plays a role in the body's physiological and pathological processes. The current study confirmed that there were at least two of genes encoding COX in cells, namely COX-1 and COX-2. COX-2 has been called the "rapid-response genes" or inducing immediateearly gene. Under normal physiological conditions COX-2 is almost not expressed or expressed very little, but when various growth factor, cytokines, inflammation, tumor factors, hormone and mitogen so on stimulus COX-2 to fast express, participate in various pathophysiological events.Recent research have shown that COX-2 was not only with pathophysiological events, but also with the occurrence and development of tumor closely linked. Wnt signaling pathway regulates cells'growth, movement and differentiation, and has been identified as a key tumor-related signaling pathway. APC gene cloning protein / adenomatous polyposis coli protein is a member of the Wnt signaling pathway, the change of adenomatous polyposis coligene can not only cause of familial adenomatous polyposis, and is involved in sporadic colorectal cancer formation. In recent years, with the improvement of molecular biology techniques, APC involved in the occurrence and development of colorectal cancer, its mechanisms was researched continuing in-depth.In the experiment by detecting the expression of COX-2 and APC in colorectal carcinoma, cancer adjacent tissues and normal colorectal mucosa tissue, the paper studied the correlation between COX-2 and APC, and discused the role of COX-2 and APC in development of colorectal cancer genesis and the relationship between with clinicopathological parameters.Methods: The expression of COX-2 and APC about 45 cases of colorectal cancer,the corresponding proximal adjacent tissues (3cm from the cancer tissue) and 30 cases of normal colorectal tissues were detected using immunohistochemistry SP (Peroxidase streptavidin tag) method.,and the comprehensive analysis of combined the patient's age,sex,tumor size,location,infiltration depth,differentiation degree,lymph node metastasis and Dukes stage and other clinicopathological factors so on . SPSS13.0 statistical software used for statistical data processing,χ2 test count data(P < 0.05 significant difference). It analysed the relationship between the expression of both COX-2 and APC in colorectal cancer by using Spearman rank correlation which is one of non-parametric statistics. The reagents: COX-2 mouse anti-human monoclonal antibody was the product of the U.S. LABVISION, and it's working concentration 1:100; concentrated anti-APC rabbit polyclonal antibody C-20 was the product of the United States Santa Cruz, its working concentration 1:200. SP immunohistochemistry kit, DAB kits were purchased in Beijing Zhong Shan Golden Bridge Biotechnology Co., Ltd. Results: 1 The expression of COX-2 and APC between colorectal carcinoma and control groups1.1 The expression of COX-2 in colorectal cancer was high: the positive expression of COX-2 in colorectal cancer was 86.7% in the cancer tissues,51.1% in proximal cancer tissues and 10.0% in the normal mucosa. The expression of COX-2 in cancer tissues was significantly higher than the proximal adjacent tissues and normal colorectal tissue (P<0.05, significant difference), and the expression in the proximal adjacent tissue was significantly higher than normal mucosa (P <0.05, significant difference).1.2 The expression of APC in colorectal cancer was low: the positive expression rate was 40.0% in the cancer tissues, 51.1% in proximal cancer tissues and 96.7% in the normal mucosa. The expression of APC in normal colorectal tissues were significantly higher than proximal cancer tissues and cancer tissues (P<0.05, significant difference), and the expression of APC in Cancer tissues and proximal adjacent tissues was no significant difference (P >0.05).2 The relationship between the expression of both COX-2 and APC in colorectal cancer and the Clinical pathology characteristic of colorectal cancer2.1 The positive expression of COX-2 in differentiated and well-differentiated colorectal cancer was 66.7%, and it was significantly lower than in poorly differentiated colorectal cancer in which The positive expression of COX-2 was 96.7% (P<0.05). The positive expression of COX-2 in infiltrating muscularis of the colorectal cancer, was 75.0% and 100% in baptist serosa of the colorectal cancer, there was a significant difference between them (P<0.05).The positive expression of COX-2 in the colorectal cancer without lymph node metastasis was 70.6%, and it was a significantly lower than in colorectal cancer with lymph node metastasis in which the positive expression of COX-2 was 96.4% (P<0.05). The positive expression of COX-2 in Dukes staging of A + B stage colorectal cancer was 70.6%, and it was a significantly lower than in Dukes staging of C + D stage colorectal cancer in which the positive expression of COX-2 was 96.4% (P<0.05).The expression of COX-2 had no significant relationship with colorectal cancer patient's age, sex, tumor size and tumor location (P >0.05).2.2 The positive expression of APC in differentiated and well-differentiated colorectal cancer was 80.0%, and it was significantly lower than in poorly differentiated colorectal cancer in which The positive expression of APC was 20.0%(P<0.05). The expression of APC had no significant relationship with colorectal cancer patient's age,, sex, tumor size, tumor location, depth of invasion, Dukes stage and lymph node metastasis(P >0.05).3 The relationship between the expression of COX-2 and APC in colorectal cancerUsing Spearman rank correlation analysis indicated that the COX - 2 and APC protein expression in colorectal tissues negatively correlated (r = - 0.626, P < 0.05).Conclusion: (1) The expression of COX-2 in colorectal cancer was high, and it was closely related to tumor differentiation, depth of invasion, Dukes stage and lymph node metastasis. The expression of COX-2 in poorly differentiated colorectal carcinoma was higher than in differentiated and well-differentiated colorectal cancer. The expression of COX-2 in baptist serosa of the colorectal cancer was higher than in infiltrating muscularis of the colorectal cancer. The expression of COX-2 in Dukes staging of C+D stage colorectal cancer was higher than in Dukes staging of A + B stage colorectal cancer. The expression of COX-2 in colorectal cancer with lymph node metastasis was higher than in the colorectal cancer without lymph node metastasis.(2) APC in colorectal cancer tissues showed lower expression, and it was closely related tothe degree of tumor differentiation. The expression of APC in differentiated and well-differentiated colorectal cancer was significantly higher than in poorly differentiated colorectal cancer. (3) The expression of COX-2 and APC in colorectal carcinoma was negatively correlated, COX-2 may be another new target gene by which APC gene mutations leads to abnormal Wnt pathway, COX-2 and APC both play an important role in the occurrence and development of colorectal cancer. |
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