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

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

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。

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.