Zhang Zhengliang, Sun Jiangli, Bai Zhenghai, Li Haijun, He Shicai, Chen Rui, Che Xiangming
Department of Emergency, Second Affiliated Hospital, Xi'an Jiaotong University, Xi'an 710004, China.
Department of General Surgery, First Affiliated Hospital, Xi'an Jiaotong University, Xi'an 710061, China.
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2015 May;31(5):672-6.
To investigate the expression of FOXA2 in human gastric adenocarcinoma and its correlation with cell migration and invasion.
Fifty-six pairs of gastric adenocarcinoma and matched tumor-adjacent tissues were freshly collected. The expressions of FOXA2 and epithelial cadherin (E-cadherin) in the gastric specimens were detected using immunohistochemistry. Western blotting was performed to test FOXA2 and E-cadherin expressions in different gastric cancer cell lines. FOXA2 was over-expressed in MKN-45 cells. TranswellTM assays were performed to observe gastric cancer cell migration and invasion in vitro. Spearman rank correlation coefficient was used for correlation analysis.
The expressions of FOXA2 and E-cadherin in gastric adenocarcinoma were significantly lower than those in matched tumor-adjacent noncancerous tissues. FOXA2 was positively correlated with E-cadherin expression in gastric adenocarcinoma tissues. Clinical analysis suggested that FOXA2 expression was prominently associated with tumor differentiation, infiltration depth, lymph node metastasis and TNM stage, respectively. The lowest expressions of FOXA2 and E-cadherin were found in highly invasive gastric cancer MKN-45 cell line; the highest expressions of FOXA2 and E-cadherin were observed in low metastatic gastric cancer N-87 cell line. Over-expression of FOXA2 significantly increased the expression of E-cadherin protein and obviously inhibited cell migration and invasion in MKN-45 cells.
Expression of FOXA2 is reduced in gastric adenocarcinoma tissues and its low-expression is correlated with malignant clinical pathological features. Over-expression of FOXA2 in MKN-45 cells up-regulates E-cadherin expression and inhibits gastric cancer cell migration and invasion.
研究叉头框蛋白A2(FOXA2)在人胃腺癌中的表达及其与细胞迁移和侵袭的相关性。
新鲜收集56对胃腺癌组织及其配对的癌旁组织。采用免疫组织化学法检测胃标本中FOXA2和上皮钙黏蛋白(E-cadherin)的表达。运用蛋白质免疫印迹法检测不同胃癌细胞系中FOXA2和E-cadherin的表达。在MKN-45细胞中过表达FOXA2。采用TranswellTM实验观察胃癌细胞的体外迁移和侵袭能力。采用Spearman等级相关系数进行相关性分析。
胃腺癌中FOXA2和E-cadherin的表达明显低于其配对的癌旁非癌组织。在胃腺癌组织中,FOXA2与E-cadherin表达呈正相关。临床分析表明,FOXA2表达分别与肿瘤分化、浸润深度、淋巴结转移及TNM分期显著相关。在高侵袭性胃癌MKN-45细胞系中,FOXA2和E-cadherin的表达最低;在低转移性胃癌N-87细胞系中,FOXA2和E-cadherin的表达最高。在MKN-45细胞中过表达FOXA2可显著增加E-cadherin蛋白的表达,并明显抑制细胞的迁移和侵袭。
胃腺癌组织中FOXA2表达降低,其低表达与恶性临床病理特征相关。MKN-45细胞中FOXA2过表达可上调E-cadherin表达并抑制胃癌细胞的迁移和侵袭。