沉默信息调节因子-1及上皮性钙黏附素在胃癌中的表达及其相关性

目的:探讨沉默信息调节因子-1(silence signal regulating factor-1，SIRT-1)和上皮性钙黏附素(epithelial cadherin，E-cadherin)在胃癌组织中的表达及其相关性。方法:采用HE 染色观察正常胃黏膜组织及癌组织的病理结构；采用免疫组织化学方法检测SIRT-1和E-cadherin在正常胃黏膜组织及癌组织中的表达水平;Spearman相关检验检测SIRT-1 与E-cadherin 表达的相关性。结果:HE 染色结果:胃癌组织中癌细胞分化差，多形性，大小不一，可呈假复层，核大，胞浆少，容易找到核分裂。免疫组织化学检测结果:SIRT-1在正常胃黏膜组织和胃癌组织的阳性表达率分别为40.5%和64.3%;E-cadherin 的阳性表达率分别为73.8%和40.5%。两组SIRT-1和E-cadherin的阳性表达率差异有统计学意义（P<0.05）。Spearman相关分析显示SIRT-1 与E-cadherin 的表达水平呈负相关（P<0.05）。胃癌组织中SIRT-1蛋白阳性表达与肿瘤大小及病理类型有关（P<0.05）；而与患者的年龄、性别、TNM分期及淋巴结转移无关（P>0.05）。结论:胃癌组织中SIRT-1高表达可能通过抑制E-cadherin促使肿瘤组织细胞发生侵袭、转移。

The expressions and relationship of SIRT-1 and E-cadherin in gastric cancer

Objective:To research the expressions and relationship of silence signal regulating factor-1(SIRT-1) and epithelial cadherin(E-cadherin) in gastric cancer.Methods:HE staining was used to observe the histopathologic structure in the cancer group and normal gastric mucosa group.Immunohistochemistry SP technique was used to detect the expressions of SIRT-1 and E-cadherin in cancer group and normal gastric mucosa group.Spearman correlation test was used to detect the expression correlation of SIRT-1 and E-cadherin.Results:HE staining gastric cancer tissue:Cell differentiation was poor,pleomorphism and different size.Cells showed fake many layers,cell nucleus was large and karyokinesis,kytoplasm was few.The immunohistochemistry showed the positive expression of SIRT-1 were 40.5% and 64.3% in the normal gastric mucosa group and cancer group.The positive expression rate of E-cadherin were 73.8% and 40.5% respectively in the normal gastric mucosa group and cancer group(P<0.05).Spearman correlation test showed that there was a correlation between SIRT-1 and E-cadherin(P<0.05).SIRT-1 protein expression was related to the tumor size and pathological types(P<0.05).But not related to the age,gender，TNM stage and lymph node metastasis(P>0.05).Conclusion:Gastric cancer with the higher SIRT-1 expression may be the ways to achieve tumor invasion and metastasis through E-cadherin as a facilitator.