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作 者:王卫华[1] 王昌正[1] 蒋一[2] 吴本俨[1]
机构地区:[1]解放军总医院老年消化内科,北京100853 [2]解放军总医院口腔科,北京100853
出 处:《南方医科大学学报》2014年第12期1748-1752,共5页Journal of Southern Medical University
基 金:国家自然科学基金(81070296)~~
摘 要:目的探讨mi R-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mi R-92b inhibitor和mi R-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mi R-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mi R-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 mi R-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。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.
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