| Objective:Colorectal cancer (colorectal cance, CRC) is a common malignant tumor of the digestive tract. In recent years, data show that as people around the improvement of living standards, changes in diet, the incidence rate showed an increasing tendency, especially in China and other developing countries, the incidence increased significantly.colorectal cancer development is a complex process, including intestinal epithelial cell proliferation, differentiation and apoptosis such as multi-stage process disorder. Many studies have confirmed the occurrence of gastrointestinal tumors and signaling pathway abnormalities are closely related. Therefore, the signal transduction pathway is to investigate the mechanism of cancer, to find effective preventive measures, early detection of cancer, early diagnosis and early treatment to reduce the morbidity and mortality in the key.Wnt signaling pathway is the cell signal transduction pathways of research. Wnt signaling pathway is the regulation of cell growth, development and differentiation of the critical pathway. Oncogenes, tumor suppressor genes or mutations in components of Wnt signaling pathway that is not properly activate this pathway, and tumor occurrence and development, in particular, is closely related with gastrointestinal tumors.Pathogenesis of colorectal cancer study, cyclooxygenase -2 is also a hot spot in recent years. COX-2 is a synthesis of prostaglandins of the rate-limiting enzyme, can be involved in regulation of cell proliferation, differentiation, inhibition of apoptosis and other ways to promote tumor development and progression, and overexpression of COX-2 can enhance tumor And transfer of potential , thereby increasing the invasiveness of tumor cells. This study was designed through the normal colorectal tissue, colorectal cancer COX-2, c-myc,β-catenin and survivin detection in order to observe COX-2, c-myc,β-catenin and survivin in normal colorectal Rectum and colorectal cancer tissues. Analysis of COX-2, c-myc,β-catenin and survivin in patients with colorectal cancer by age, sex, tumor overview, differentiation and Dukes stage, lymph node metastasis correlation between clinicopathological features and mutual relations. Of Wnt pathway and COX-2 in colorectal tumorigenesis and their relationship to the incidence of colorectal cancer, prevention and treatment to provide a new theoretical basis and experimental basis.Methods: Immunohistochemical (peroxidase labeled streptavidin-avidin method) in 50 cases of colorectal cancer and 30 normal colorectal tissues for COX-2 and c-myc,β-catenin and survivin protein expression detection, and With the patient's age, gender, tumor size, location, depth of invasion, differentiation, Dukes stage and lymph node metastasis and other clinicopathological factors were analyzed.Results:1 The expression of COX-2, c-myc, beta catenin and surviving:1.1 COX-2 in colorectal cancer showed high expression, the positive rate was 88.0% (44/50), normal colorectal tissues was 13.3% (4/30). COX-2 expression in cancer tissues was significantly higher than that of normal colorectal tissue (P <0.05).1.2 c-myc in colorectal cancer showed high expression, the positive rate was 68.0% (34/50), normal colorectal tissues was 10.0% (3/30). c-myc expression in cancer tissues was significantly higher than that of normal colorectal tissue (P <0.05);1.3 survivin in colorectal cancer showed high expression, the positive rate was 66.0% (33/50), normal colorectal tissues was 3.3% (1/30), survivin expression in cancer tissues was significantly higher than in normal colorectal tissue (P <0.05).1.4β-catenin in the cytoplasm of colorectal cancer and / or ectopic expression of nucleus was 90.0% (45/50), normal colorectal tissues was 16.7% (5/30).β-catenin in the cytoplasm in cancer tissues and / or nucleus of ectopic expression was significantly higher than that of normal colorectal tissue (P <0.05);2 The relationship of COX - 2, c - myc, beta catenin and survivin expression and colorectal cancer clinical parameters:2.1 COX-2 in the low undifferentiated expression in colorectal cancer was 97.0% (32/33) was significantly higher than the high differentiation of colorectal cancer positive rate 70.6% (12/17) (P <0. 05) ; COX-2 in colorectal cancer invading the serosa positive expression rate of 100% (24/24) was significantly higher than that of colorectal cancer invading the muscle tissue 76.9% (20/26) (P <0.05); COX-2 in Dukes C + D phases of positive expression in colorectal cancer was 96.7% (29/30) than Dukes stage was A + B stage colorectal cancer 75.0% (15/20 ) (P <0.05); COX-2 in colorectal cancer with lymph node metastasis positive expression rate was 100% (32/32) was significantly higher than that of lymph node metastasis of colorectal cancer positive rate of 66.7% (12/18) (P <0.05) .the expression of COX - 2 in colorectal cancer patients with colorectal cancer age, sex, tumor size, and tumor location were not significantly related (P > 0.05).2.2 c-myc in colorectal cancer invading the serosa positive expression ratwas83.3% (20/24) was significantly higher than that of colorectal cancer invading the muscle tissue 53.8% (14/26) (P <0.05). c-myc in Dukes C + D phases of positive expression in colorectal cancer was 76.7% (23/30) than Dukes stage was A + B stage colorectal cancer 55.0% (11/20) (P <0.05). c-myc in colorectal cancer with lymph node metastasis positive expression rate was 84.4% (27/32) was significantly higher than that of lymph node metastasis of colorectal cancer 38.9% (7 / 18) (P <0.05).c -myc expression and colorectal cancer patient's age, gender, tumor size, tumor location and tumor differentiation degree were not significantlyrelated (P > 0.05).2.3β-catenin in colorectal cancer with lymph node metastasis positive expression rate was 100% (32/32) was significantly higher than that of lymph node metastasis in colorectal cancer 72.2% (13/18)(P<0.05).β-catenin expression in colorectal cancer patients with the age, sex, tumor size, tumor location, tumor depth of invasion and Dukes stage had no significant correlation (P> 0.05).2.4 survivin in poorly differentiated and undifferentiated expression in colorectal cancer was 72.7% (24/33) than in well and moderately differentiated colorectal cancer tissue 52.9% (9/17) (P<0.05).survivin expression in colorectal cancer with age, sex, tumor size, tumor location, depth of invasion, Dukes stage and lymph node metastasis had no significant correlation (P> 0.05).3 The correlation of COX-2, c-myc,β-catenin and survivin protein in colorectal carcinoma3.1 In colorectal cancer the expression of COX-2 and the expression of c-myc,β-catenin, survivin was positively correlated(P<0.05), the correlation coefficient r = 0.894,0.447,0.386. With the expression of c-myc,β-catenin and survivin protein increased, the expression of COX-2 protein increased.3.2β-catenin in colorectal cancer tissue and c-myc, survivin protein in colorectal cancer tissues showed a positive correlation(P<0.05) coefficient of r =0.884,0.457.With the increased expression ofβ-catenin protein, the expression of c-myc, survivin protein were significantly increased.3.3 c-myc and survivin protein expression in colorectal cancer was positively correlated (P <0.05), correlation coefficient r = 0.929.Conclusions:1 Abnormal activation of Wnt signaling pathway and colorectal cancer occurrence and development of close, and colorectal cancer tumor differentiation, tumor invasion and lymph node metastasis.2 COX-2 is closely related with the degree of differentiation,depth of invasion,Dukes stage and lymph node of colorectal cancer.3 In colorectal cancer, the expression of COX-2 and the expression of c-myc, beta-catenin and survivin protein was positively correlated; COX-2 may be an abnormal Wnt pathway downstream target genes; In-depth study on the relationship between the two future colorectal cancer early detection and prevention of significant value.
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