NR2F2过表达对三阴性乳腺癌细胞迁移、侵袭的影响及机制研究

Effect and Mechanism of NR2F2 Overexpression on Migration and Invasion of Triple Negative Breast Cancer Cells

目的阐明NR2F2对三阴性乳腺癌细胞迁移、侵袭的影响及其可能的机制。方法采用慢病毒感染构建稳定高表达NR2F2的小鼠乳腺癌4T1细胞株。划痕实验和Transwell迁移和侵袭实验分别检测细胞的迁移和侵袭能力。实时荧光定量聚合酶链式反应(Real-time PCR)和蛋白免疫印迹法(Western blot)检测细胞中NR2F2、E-cadherin、N-cadherin、Vimentin的mRNA和蛋白的表达情况。结果三阴性乳腺癌4T1细胞过表达NR2F2后,细胞的迁移和侵袭能力增强,间质表型标志物N-cadherin、Vimentin表达升高,上皮表型标志物E-cadherin表达降低。结论NR2F2通过诱导三阴性乳腺癌细胞上皮间质转化,促进了细胞的迁移和侵袭。针对NR2F2的靶向干预可望为治疗三阴性乳腺癌提供新的策略。

Objective To clarify the effect and possible mechanism of NR2 F2 on the migration and invasion of triple negative breast cancer cells.Methods A mouse triple negative breast cancer 4 T1 cell strain stably over-expressing NR2 F2 was constructed.The wound-heal assay,transwell migration and invasion assay were applied to detect the migration and invasion ability of cells.The mRNA and protein expression levels of NR2 F2,E-cadherin,N-cadherin,Vimentin in cells were measured by real-time quantitative polymerase chain reaction(Real-time PCR)and Western blotting,respectively.Results In 4 T1 cells,the migration and invasion ability were increased by NR2 F2 overexpression.The expression levels of mesenchymal phenotypic markers including N-cadherin and Vimentin,were increased,while epithelial phenotypic marker E-cadherin decreased after NR2 F2 overexpression.Conclusion NR2 F2 promotes migration and invasion of cells by inducing epithelial-mesenchymal transition in triple negative breast cancer cells.These may provide new strategies of treatment for triple negative breast cancer patients.