miR-92b 对人胃癌细胞SGC7901迁移、粘附和侵袭的影响

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。

Effect of miR-92b on migration,adhesion and invasion of human gastric cancer cell line SGC7901

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.