环氧合酶-2对人SGC-7901胃癌细胞E-cadherin的表达及迁移能力的影响

目的 研究环氧合酶-2（COX-2）通过调控E-钙黏素（E-cadherin）对胃癌细胞侵袭迁移能力的影响。方法 分别应用塞来昔布（Celecoxib）及前列腺素E2(PGE2)对体外培养的人胃癌细胞SGC-7901进行干预，采用实时荧光定量反转录PCR检测COX-2、E-cadherin mRNA的表达；运用免疫荧光标记法结合激光共聚焦荧光显微镜分析E-cadherin的蛋白表达量；应用Transwell法检测细胞迁移能力的变化。结果 实时荧光定量反转录PCR检测塞来昔布明显抑制体外培养人胃癌细胞SGC-7901中COX-2 mRNA的表达（P＜0.01），而E-cadherin mRNA的表达随着COX-2的表达下降而呈浓度与时间依赖性升高（P＜0.01）；运用PGE2干预后E-cadherin mRNA表达呈浓度与时间依赖性下降（P＜0.05或P＜0.01）。塞来昔布30 μmol/L干预人胃癌细胞SGC-7901 24、36、48 h后，激光共聚焦荧光显微镜检测E-cadherin的蛋白表达量明显升高（P＜0.05）；PGE2 1 μmol/L干预24、48 h后，E-cadherin蛋白表达量明显下降（P＜0.05）。塞来昔布组穿过Transwell小室的细胞数明显少于对照组（P＜0.01），PGE2组穿过Transwell小室的细胞数明显高于对照组（P＜0.05）。结论 COX-2特异性抑制塞来昔布通过抑制COX-2的表达，上调E-cadherin表达量，抑制体外培养人胃癌细胞SGC-7901的迁移能力；外源性PGE2能够下调SGC-7901胃癌细胞E-cadherin表达量从而促进肿瘤细胞的迁移能力。

Effects of Cyclooxygenase-2 on E-cadherin Expression and Migration of Human Gastric Carcinoma Cell Line SGC-7901 in vitro

Objective To investigate the effects of cyclooxygenase-2(COX-2) regulating E-cadherinexpression on migration capability of gastric carcinoma cell line SGC-7901.Methods After SGC-7901cell line treated by Celecoxib and PGE2 in vitro, real-time quantitative PCR was used to detect the changesof mRNA levels of COX-2 and E-cadherin. The combination of immunofluorescence and Confocal laserscanning microscopy was used to analyze the protein level of E-cadherin. Transwell was used to detect thechange of cell migration.Results COX-2 mRNA expression was inhibited by Celecxib, but E-cadherinmRNA expression level was increased signifi cantly with decreased COX-2 expression, in a dose- and timedependentmanner(P＜0.01).On the contrary, E-cadherin mRNA expression level was decreased in a timeanddose-dependent manner after PGE2 treatment(P＜0.05 or P＜0.01). After SGC-7901 cell line were treatedwith Celecxib (30 μmol/L) for 24,36,48 h, E-cadherin protein level was increased significantly(P＜0.05),while E-cadherin protein expression was signifi cantly decreased after PGE2 treatment(1 μmol/L) for 24 and 48h (P＜0.05).The cell numbers through Transwell with Celecoxib treatment was less than that of no-treatmentgroup(P＜0.01).While, the cell numbers through Transwell with PGE2 treatment was more than that of notreatmentgroup (P＜0.05).Conclusion Celecoxib, selective COX-2 inhibitor, may upregulate E-cadherinexpression and inhibit the invasive potential of human gastric carcinoma by suppressing COX-2 expression.PGE2 may downregulate E-cadherin expression and promote the migration of SGC-7901 in vitro.