| Objective:To investigate the regulation and significance ofβ-catenin,E-cadherin and CyclinD1 in gastric carcinoma and study the role of the correlation between them for the clinical diagnosis and provide usefull prognostic indicator.Methods:Selecting 70 cases of paraffin block filed by Department of Pathology, Affiliated Hospital of Luzhou Medical College from October 2008 to October 2009,including 20 cases of dysplasia,among which 10 cases were moderate dysplasia,10 cases were severe dysplasia;50 cases of advanced gastric adenocarcinoma, among which 15 cases were differentiated type,15 cases were well differentiated type and 20 cases were poorly differentiated type.At the same time,selecting 20 cases of normal gastric tissue 5cm away from carcinoma tissue as control group. Each specimen, histological type was confirmed by pathological diagnosis.The expression ofβ-catenin, E-cadherin and cyclinD1 was detected in 20 cases of normal gastric tissues,20 cases of dysplasia and 50 cases of gastric carcinoma by immunohistochemistry S-P method.Using SPSS 15.0 for statistical analysis, count data was analyzed by chi-square test and Fisher exact probabilities test.Multi-factor Binary Logistic regression analyzed correlation betweenβ-catenin, E-cadherin and CyclinD1 with pathologic parameters, and correlation analysis was made by Spearman rank correlation analysis.Results:(1)The missing expression rates ofβ-catenin in the normal gastric tissue,dysplasia and gastric carcinoma were 0%,40.0%, 68.0% respectively.The missing expression rate ofβ-catenin in the gastric carcinoma was significantly higher than that in the normal gastric tissue and dysplasia(x2=26.44, P<0.001; x2=4.67, P＜0.05). The missing expression rate ofβ-catenin in the dysplasia was significantly higher than that in the normal gastric tissue(x2= 10.00, P＜0.01); The missing expression rate of E-cadherin in the normal gastric tissue,dysplasia and gastric carcinoma were 0%,10.0%,56.0% respectively.The missing expression rate of E-cadherin in the gastric carcinoma was significantly higher than that in the normal gastric tissue and dysplasia (x2= 18.67, P＜0.001;x2=12.34, P<0.001).There was no significant difference between normal gastric tissue and dysplasia(P>0.05); The positive expression rates of CyclinD1 in the normal gastric tissue,dysplasia and gastric carcinoma were 0%,25.0%,62.0% respectively.The positive expression rate of E-cadherin in the gastric carcinoma was significantly higher than that in the normal gastric tissue and dysplasia(x2=22.26, P＜0.001; x2=7.83, P<0.01).There was no significant difference between normal gastric tissue and dysplasia (P>0.05). (2)The expression ofβ-catenin was closely related to the grade of cell differentiation, depth of invasion and lymph node metastasis of gastric carcinoma(P<0.05).There was no correlation between the expression ofβ-catenin and sex,age of the patients and tumor size of gastric carcinoma; The expression of E-cadherin was closely related to tumor size, grade of cell differentiation, depth of invasion and lymph node metastasis of gastric carcinoma(P<0.05).There was no correlation between the expression of E-cadherin and sex and age of the patients; The expression of CyclinD1 was closely related to tumor size, grade of cell differentiation, depth of invasion and lymph node metastasis of gastric carcinoma(P<0.05).There was no correlation between the expression of CyclinD1 and sex and age of the patients.Logistic regression analysis showed that tumor size and infiltration depth were independent related factors of the expression ofβ-catenin, lymph node metastasis was an independent related factor of the expression of E-cadherin. (3)There was positive correlation between P-catenin and E-cadherin in gastric carcinoma(r=0.667, P=0.000).There was no significant correlation betweenβ-catenin and CyclinD1 in gastric carcinoma(r=-0.027,P=0.092).There was no significant correlation between E-cadherin and CyclinD1 in gastric carcinoma (r=-0.329,P=0.014).Conclusions:(1)The expression ofβ-catenin in gastric cancinoma is significantly lower than that in the normal gastric mucosa and dysplasia, and the expression of P-catenin in dysplasia is significantly lower than that in the normal gastric mucosa.The expression ofβ-catenin is associated with tumor differentiation, invasion depth and lymph node metastasis. Detection ofβ-catenin expression can be used as an early indicator in diagnosis and prognosis of gastric carcinoma.(2)The expression of E-cadherin in gastric cancinoma is significantly lower than that in the normal gastric mucosa and dysplasia, suggesting that abnormal expression of E-cadherin may be associated with the occurrence of gastric cancinoma.Meanwhile,the abnormal expression of E-cadherin may be associated with the tumor size, differentiation, invasion depth,and lymph node metastasis, suggesting that the abnormal expression of E-cadherin may play an important role in the spread of the cancer which makes it a potential value in the prediction of metastasis of gastric carcinoma. (3)The expression of CyclinD1 in normal gastric mucosa, dysplasia and gastric cancinoma increase gradually, and that is the same from well-differentiated carcinoma to poorly differentiated cancer, without serosal cancer invasion to serosal cancer, without metastasis to metastasis, indicating that the higher expression of CyclinD1 is associated with the higher malignant tumor and the higher probability of metastasis.It is suggested that the expression of CyclinD1 plays an important role in the occurrence and development of the gastric cancinoma and in the assessment of prognosis. (4)The expression ofβ-catenin and E-cadherin in gastric cancinoma is positively correlated, suggesting that the abnormal E-cadherin/catenins complex is also involved in gastric carcinogenesis which may be one of the key steps of malignant phenotype. E-cadherin not only can serve as a member of the E-cadherin/catenins complex involved in cell adhesion, but it can also interact with Wnt pathways by P-catenin, and affect the process of invasion and metastasis of gastric cancinoma by affecting (3-catenin intracellular distribution.
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