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AIM:To investigate maspin expression in tumorigenesis andprogression of gastric cancer and to explore its relevantmolecular mechanisms.METHODS:Formalin-fixed and paraffin-embedded tissuesfrom normal mucosa (n=182),dysplasia (n=69),cancer(n=113) of the stomach were studied for maspin expressionby immunohistochemistry.Microvessel density (MVD) ingastric cancer was labeled using anti-CD34 antibody.Maspinexpression was compared with clinical parameters and MVDof tumors.Caspase-3 expression was also detected in gastriccarcinoma by immunohistochemistry.The relationshipbetween Caspase-3 and maspin expression was concernedas well.RESULTS:The positive rates of maspin expression were79.8%(145/182),75.4%(52/69) and 50.4%(57/113)innormal mucosa,dysplasia and cancer of the stomach,respectively.Cancer less frequently expressed maspin thannormal mucosa and dysplasia (P<0.05).Maspin expressionshowed a significantly negative association with invasivedepth,metastasis,Lauren’s and Nakamura’s classification(P<0.05),but not with tumor size,Borrmann’s classification,growth pattern or TNM staging (P>0.05).The positive rateof Caspase-3 was significantly lower in gastric cancer thanin normal gastric mucosa (P<0.05,32.7% vs50.4%).It wasnoteworthy that maspin expression was negatively correlatedwith MVD,but positively correlated with expression ofCaspase-3 in gastric cancer (P<0.05).CONCLUSION:Down-regulated maspin expression is a latemolecular event in gastric carcinogenesis.Reduced expressionof maspin contributes to progression of gastric cancerprobably by inhibiting cell adhesion,enhancing cell mobility,decreasing cell apoptosis and facilitating angiogenesis.Additionally altered expression of maspin underlies themolecular mechanism of differentiation of gastric cancer andsupports the different histogenetic pathways of intestinaland diffuse gastric cancers.Maspin expression can beconsidered as an effective and objective marker to revealbiological behaviors of gastric cancer.
AIM: To investigate maspin expression in tumorigenesis andprogression of gastric cancer and to explore its relevantmolecular mechanisms. METHODS: Formalin-fixed and paraffin-embedded tissues from normal mucosa (n = 182), dysplasia (n = 69), cancer of the stomach were studied for maspin expressionby immunohistochemistry. Microvessel density (MVD) ingastric cancer was labeled using anti-CD34 antibody. Maspinexpression was compared with clinical parameters and MVD of tumors. Caspase-3 expression was also detected in gastriccarcinoma by immunohistochemistry. The relationship between Caspase -3 and maspin expression was concerned as well .RESULTS: The positive rates of maspin expression were 79.8% (145/182), 75.4% (52/69) and 50.4% (57/113) innormal mucosa, dysplasia and cancer of the stomach, respectively. Cancer less frequently expressed maspin than normal mucosa and dysplasia (P <0.05). Maspin expressions showed a significant negative association with invasive disease, metastasis, Lauren’s and Nakamura’s classificati (P <0.05), but not with tumor size, Borrmann’s classification, growth pattern or TNM staging (P> 0.05) .The positive rate of Caspase-3 was significantly lower in gastric cancer than normal gastric mucosa vs was 50.4%). It wasnoteworthy that maspin expression was negatively correlated with MVD, but positively correlated with expression of Caspase-3 in gastric cancer (P <0.05) .CONCLUSION: Down-regulated maspin expression is a latemolecular event in gastric carcinogenesis. Reduced expression of maspin contributes to progression of gastric cancer bacteria by inhibiting cell adhesion, enhancing cell mobility, decreasing cell apoptosis and facilitating angiogenesis. Adlated altered expression of maspin underlies themolecular mechanism of differentiation of gastric cancer and support the different histogenetic pathways of intestinaland diffuse gastric cancers. Maspin expression can beconsidered as an effective and objective marker to revealbiological behaviors of gastric cancer.