CAJ | 학술논문

目的：探讨miR-92b对胃癌细胞迁移、粘附和侵袭能力的影响及其相关的分子机制。方法在人胃癌SGC-7901细胞中瞬时转染miR-92b inhibitor和miR-92b mimics后，经划痕实验、细胞迁移实验、基质胶粘附实验和Transwell侵袭实验观察对细胞转移的影响；Western blot检测E-Cadherin、Vimentin、Akt和p-Akt蛋白的表达水平。结果 SGC-7901细胞转染miR-92b inhibitors后，迁移、粘附和侵袭的细胞数量减少（P<0.05）；Western blot结果显示E-Cadherin表达升高，Vimentin表达降低，Akt和p-Akt的表达升高。转染miR-92b mimics后，迁移、粘附和侵袭的细胞数量增多（P<0.05）；E-Cadherin表达降低，Vimentin表达升高，Akt和p-Akt表达降低。结论 miR-92b介导SGC7901细胞发生上皮-间质转化，促进肿瘤细胞的粘附、迁移和侵袭，可能通过非PI3K/Akt途径促进肿瘤细胞的转移。
목적：탐토miR-92b대위암세포천이、점부화침습능력적영향급기상관적분자궤제。방법재인위암SGC-7901세포중순시전염miR-92b inhibitor화miR-92b mimics후，경화흔실험、세포천이실험、기질효점부실험화Transwell침습실험관찰대세포전이적영향；Western blot검측E-Cadherin、Vimentin、Akt화p-Akt단백적표체수평。결과 SGC-7901세포전염miR-92b inhibitors후，천이、점부화침습적세포수량감소（P<0.05）；Western blot결과현시E-Cadherin표체승고，Vimentin표체강저，Akt화p-Akt적표체승고。전염miR-92b mimics후，천이、점부화침습적세포수량증다（P<0.05）；E-Cadherin표체강저，Vimentin표체승고，Akt화p-Akt표체강저。결론 miR-92b개도SGC7901세포발생상피-간질전화，촉진종류세포적점부、천이화침습，가능통과비PI3K/Akt도경촉진종류세포적전이。
Objective To investigate the effect of miR-92b on the migration, adhesion and invasion of gastric cancer cell line SGC7901. Methods The miR-92b inhibitor and mimics were transiently transfected in SGC7901 cells. The changes in the migration, adhesion and invasion of the transfected cells were tested with wound healing assay, Transwell migration assay, matrigel adhesion and Transwell invasion assay. The cellular expression of E-cadherin, vimentin, Akt and p-Akt were analyzed by Western blotting. Results The migration, adhesion and invasion assays showed that transfection with the inhibitor of miR-92b obviously decreased the numbers of gastric cancer cells. The expression of E-cadherin, AKT, and pAKT increased and vimentin decreased significantly in the cells transfected with the inhibitor of miR-92b. Transfection with the mimics of miR-92b produced opposite effects in SGC7901 cells. Conclusion miR-92b promotes the migration, adhesion and invasion of human gastric cancer cell line SGC7901 by mediating epithelial-mesenchymal transition, and may accelerate tumor cell metastasis via signaling pathways other than PI3K/Akt pathway.