| Objective: To study the expression of COX-2, NF-κB, E-cadherin mRNA and protein in gastric carcinoma and explore the relationship between the clinical pathology and helicobacter pylori infection.Methods: 60 cases of gastric carcinoma,60 cases of precancerous tissues were chosen as experiment groups. COX-2,NF-κB and E-cadherin mRNA and protein were detected by Real-time fluorescence quantitative PCR, Immunohistochemistry staining and Western Blot.The infection of H. pylori was detected by Warthin-Starry silver stain.Results:1.The expression of COX-2, NF-κB mRNA in gastric carcinoma(8.88±4.58,2.82±1.62) was higher than that in precancerous tissues (3.65±1.92,1.61±0.95) and control (p<0.05); E-cadherin mRNA in gastric carcinoma (0.71±0.44) was lower than that in precancerous tissues (1.13±0.73) and control (p<0.05). The expression of COX-2, NF-κB and E-cadherin mRNA was no association with the clinicopathological characteristics.2. The expression of COX-2, NF-κB protein by immunohistochemistry in gastric carcinoma (60.0%,66.7%) was higher than that in precancerous tissues (35.0%,36.7%) and control (p<0.05); E-cadherin protein in gastric carcinoma (33.3%) was lower than that in precancerous tissues (70.0%) and control (p<0.05).3. The expression of COX-2, NF-κB protein by western blot in gastric carcinoma (0.59±0.32,0.88±0.43) was higher than that in precancerous tissues (0.25±0.10,0.29±0.16) and control (p<0.05);The expression of E-cadherin protein in gastric carcinoma (1.25±0.63) was lower than that in precancerous tissues (2.92±1.03) and control (p<0.05).4. In gastric carcinoma, the expression of COX-2, NF-κB protein in the differentiated gastric carcinoma(38.9%,44.4%)was lower than that in undifferentiated gastric carcinoma (69.0%,76.2%), there was significant difference between the two groups (p<0.05). the expression of COX-2, NF-κB protein in the gastric carcinoma with invasion under serosa (22.2%,33.3%) was lower than that in invasion out of serosa (66.7%,72.5%),there was significant difference between the two groups (p<0.05). The expression of E-cadherin protein in the differentiated gastric carcinoma (77.8%) was higher than that in undifferentiated gastric carcinoma (14.3%),there was significant difference between the two groups (p=0.000). The expression in invasion under serosa(66.7%) was higher than that in invasion out of serosa (27.5%),taere was significant difference between the two groups (p=0.021).5. The expression of mRNA detected by Real-time fluorescence quantitative RT-PCR displayed, there was negative correlation between COX-2 and E-cadherin(r=-0.327, p=0.011). There was positive correlation between COX-2 and NF-κB(r=0.500,p=0.000). There was negative correlation between NF-κB and E-cadherin (r=-0.267, p=0.040).6. Immunohistochemistry displayed, there was negative correlation between COX-2 and E-cadherin (r=-0.288, p=0.028). There was positive correlation between COX-2 and NF-κB (r=0.219,p=0.035). There was negative correlation between NF-κB and E-cadherin (r=-0.207, p=0.041). Western Blot displayed, there was negative correlation between COX-2 and E-cadherin (r=-0.51, p=0.022). There was positive correlation between COX-2 and NF-κB (r=0.61, p=0.004). There was negative correlation between NF-κB and E-cadherin (r=-0.601,p=0.005)7. The infection rate of H. pylori in gastric carcinoma and precancerous tissues was 76.6% and 91.7%, there was significant difference between the two groups (p=0.024).The expression of COX-2, NF-κB and E-cadherin was no correlation with the infection of H. pylori.Conclusions:1. In gastric carcinoma, COX-2,NF-κB mRNA and protein was up regulated, E-cadherin was down regulated. COX-2,NF-κB and E-cadherin was found has intimate connection with invasion and differentiation. It indicated that COX-2,NF-κB and E-cadherin play an important role in promoting the development of gastric carcinoma.2. There was negative correlation between COX-2 and E-cadherin,positive correlation between COX-2 and NF-κB, negative correlation between NF-κB and E-cadherin. These indicated that COX-2 may regulate E-cadherin expression via up-regulating NF-κB.3. The expression of COX-2, NF-κB and E-cadherin was no correlation with the infection of H. pylori.
|
PDF Full Text Request