miR-638在胃癌中的表达及其对胃癌细胞侵袭和迁移的影响

目的:探讨miR-638在胃癌中的表达，并阐释miR-638 对胃癌细胞侵袭和迁移的影响。方法:收集2013年9月至2014年9月在上海交通大学医学院附属新华医院收治的68例胃癌患者对应的癌组织及癌旁组织的成对标本，通过定量PCR检测miR-638在胃癌组织及癌旁组织中的表达情况，分析其与临床病理特征的关系。调节胃癌细胞miR-638的表达，分为增强表达组、干扰表达组和空白对照组。通过细胞划痕实验及Transwell侵袭实验，比较三组胃癌细胞的迁移及侵袭能力。结果:胃癌组织中miR-638的表达水平显著低于癌旁组织［5.637±1.214 vs 11.220±3.148（P＜0.05）］；细胞划痕实验及Transwell侵袭实验显示miR-638增强表达组较空白对照组明显抑制胃癌细胞的侵袭和迁移，而干扰组则促进胃癌细胞的侵袭和迁移（P＜0.05）。结论:miR-638在胃癌组织中的表达水平较癌旁组织显著下降，提示miR-638在胃癌组织中可能发挥抑制肿瘤的作用；miR-638的过表达抑制胃癌细胞的迁移及侵袭能力，而miR-638的下调则促进胃癌细胞的迁移及侵袭能力。

The expression of miR-638 in gastric carcinoma and its effect on invasion and migration of gastric cancer cells

Objective:To explore the expression of miR-638 in gastric carcinoma and explain the effects of miR-638 on the invasion and migratory of gastric carcinoma.Methods:A total of 68 pairs of human gastric carcinoma tissues and adjacent normal tissues were collected in Xinhua Hospital Affiliated to Shanghai Jiaotong University School of Medicine from September 2013 to September 2014 and the expression of miR-638 was detected by the method of quantitative PCR，and analyzed the relevance to their corresponding clinical pathology.The miR-638 expression was regulated in gastric cancer cells,divided into enhanced expression group,interference expression group and control group.The migration and invasion were compared by the cell invasion assay and Transwell migration assay among the above three groups.Results:The miR-638 expression in gastric carcinoma tissues was significantly lower than that in adjacent ones［5.637±1.214 vs 11.220±3.148(P＜0.05)］.Cell invasion assay and Transwell invasion assay showed that the migration in enhanced expression group was significantly inhibited compared with control group,while that ininference group was significantly promoted(P＜0.05).Conclusion:The expression level of miR-638 in gastric carcinoma was significantly lower than that in adjacent tissues,suggesting that miR-638 could play a role of tumor suppressor in gastric tissue.The migration and invasion of gastric cancer cells was inhibited by miR-638 overexpression and promoted by the downgrade of miR-638 expression.