E-cadherin和FOXO3a在胃癌组织和细胞中表达的关系

目的:探讨上皮钙黏素(E-cadherin)和叉头框蛋白O3a(FOXO3a)在胃癌组织和细胞中表达的关系及意义。方法:应用免疫组织化学法检测53例胃癌组织及对应癌旁组织中E-cadherin和FOXO3a的表达情况,分析两者的表达水平及与临床病理参数的关系。构建E-cadherin过表达的胃癌稳转细胞株AGS,免疫细胞化学法检测E-cadherin及FOXO3a蛋白表达,Western blot法检测细胞中E-cadherin、FOXO3a、Akt、Bcl-2和Bax的蛋白表达,CCK-8法检测细胞活力。结果:胃癌组织中E-cadherin和FOXO3a的阳性率较对应癌旁组织均显著降低(P0.05)。E-cadherin表达与胃癌分化程度和TNM分期显著相关(P0.05),与年龄、性别、肿瘤部位、T分期及淋巴结转移无显著相关。FOXO3a表达与胃癌分化程度显著相关(P0.05),与年龄、性别、部位、TNM分期、T期及淋巴结转移无显著相关。胃癌组织中E-cadherin与FOXO3a表达存在显著正相关(r=0.376,P=0.003)。E-cadherin过表达后,胃癌AGS细胞活力显著下降,细胞中FOXO3a和Bax表达显著升高,Akt表达显著下降。结论:E-cadherin与FOXO3a共同参与胃癌的发生发展,E-cadherin可能通过调节Akt/FOXO3a信号传导影响胃癌细胞活力。

Correlation between E-cadherin and FOXO3a expression in gastric can-cer tissues and cells

AIM: To investigate the expression of E-cadherin and forkhead box protein O3a (FOXO3a) in gastric cancer tissues and cells, and its correlation with cell viability. METHODS: The expression of E-cadherin and FOXO3a was detected by immunohistochemical staining in 53 specimens of gastric cancer tissues and their adjacent tissues, and the relationship between their expression and clinicopathological characteristics were analyzed. E-cadherin-over-expressing gastric cancer AGS cells were constructed by lentivirus-mediated cell transfection, and the protein expression of E-cadherin and FOXO3a was detected by immunocytochemistry method. The expression of E-cadherin, FOXO3a, Akt, Bcl-2 and Bax was determined by Western blot. The cell viability was detected by CCK-8 assay. RESULTS: The positive expression rates of E-cadherin and FOXO3a proteins in gastric cancer tissues were both significantly lower than those in their adjacent tissues (P<0.05). E-cadherin positive expression in gastric cancer tissues was significantly related to tumor grade and TNM stage (P<0.05), but not related to age, sex, location, T stage or lymph node metastasis. FOXO3a positive expression was significantly related to tumor grade (P<0.05), but not related to age, sex, location, TNM stage, T stage or lymph node metastasis. The expression of E-cadherin was positively correlated with FOXO3a expression in gastric cancer tissues (r=0.376, P=0.003). After over-expression of E-cadherin, the viability of gastric cancer AGS cells was significantly inhibited, the expression of FOXO3a, Bcl-2 and Bax was significantly increased, and the expression of Akt was significantly decreased. CONCLUSION: E-cadherin and FOXO3a are involved in the development of gastric cancer, and E-cadherin may affect the viability of gastric cancer cells by regulating Akt/FOXO3a signaling pathway.