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Objective To detect NKD, and Wnt2b in normal gastric mucosa to gastric expression of the development process, both in the gastric cancer study, the development process may play a role and relationship. Methods (1) SP immunohistochemical assay NKD, protein and Wnt2b in 10 cases of normal gastric mucosa, 10 cases of chronic atrophic gastritis (with intestinal metaplasia), 21 cases of dysplasia (mild, moderate and severe each 7 cases), 10 cases of early gastric cancer, 30 cases of advanced gastric cancer (high, medium and low differentiation of the 10 cases) tissues. (2) reverse transcription-polymerase chain reaction (RT-PCR) detection of seven cases of normal gastric mucosa, eight cases of dysplasia and 10 cases of gastric NKD1mRNA content. Results (1) Wnt2b in the normal mucosa and intestinal metaplasia, the positive expression rate was 0.00% (0/10) and 10.00% (1/10), Wnt2b in mild, moderate and severe dysplasia tissues rate were 14.29% (1/7), 57.14% (4/7), 71.43% (5/7), no significant difference between the three; Wnt2b expression in gastric carcinoma was 97.50% (39/40) , significantly higher than non-cancerous tissue, there was a significant difference statistically (P ≤ 0.01). (2) NKD, in normal gastric mucosa, the positive expression rate of 100.00% (10/10); intestinal metaplasia in the positive expression rate of 90.00% (9/10); in mild, moderate and severe dysplasia positive rate was 71.43% (5/7), 42.86% (3/7) and 28.57% (2/7), in which mild to moderate dysplasia and severe dysplasia was no significant difference (p gt; 0.05) ; early gastric cancer tissues NKD, positive expression rate was 10.00% (1/10), advanced gastric cancer tissues NKD, positive expression rate was 0.00% (0/10), cancerous and non-cancerous tissue group group difference was statistically significant ( p ≤ 0.01) (3) NKD1 mRNA expression in normal gastric mucosa, in dysplastic tissues weakened significantly decreased in gastric cancer (p ≤ 0.05) Conclusion (1) Wnt2b from normal gastric mucosa, intestinal metaplasia dysplasia to gastric carcinoma gradually increased, suggesting Wnt2b may regulate fine proliferation, differentiation and apoptosis processes involved in tumor development, which will lead to abnormal activation of tumorigenesis. (2) from normal gastric mucosa, intestinal metaplasia, dysplasia to early gastric cancer, NKD1 expression decreased gradually, even in advanced gastric missing. Tip NKD, Wnt signaling system may be used as the negative regulator, thus inhibiting abnormal cell proliferation. (3) non-cancerous tissues NKD1 and Wnt2b negatively correlated, suggesting NKD. Absence of Wnt signaling pathway may lead to abnormal activation.
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