Yuan Jie,Yang Li,Chen Maoshan,Zhu Qing,Fu Weijie,Cheng Hong,Liu Manran,Yang Guanglun.Identification of epithelial-mesenchymal transition phenotype in tamoxifen-resistant MCF-7 cells[J].J Amry Med Univ (J Third Mil Med Univ),2014,36(22):2272-2276.
Yuan Jie,Yang Li,Chen Maoshan,Zhu Qing,Fu Weijie,Cheng Hong,Liu Manran,Yang Guanglun.Identification of epithelial-mesenchymal transition phenotype in tamoxifen-resistant MCF-7 cells[J].J Amry Med Univ (J Third Mil Med Univ),2014,36(22):2272-2276.DOI:
Objective To investigate the changes of the cell morphology and the expression of epithelial-mesenchymal transition (EMT) marker proteins after MCF-7 cells acquired tamoxifen resistance. Methods The cell morphology was revealed through immunofluorescent staining. The expression of EMT marker proteins was detected by quantitative real-time PCR (qRT-PCR) and Western blotting. Transwell assay was used to detect the difference of cell migration. PI3K-Akt and MAPK/Erk signaling pathways were evaluated in MCF-7 cells and tamoxifen-resistant MCF-7R cells. The migration and the expression of EMT marker proteins were reevaluated after inhibiting the signaling pathways. Results In the MCF-7 cells
intercellular contact was close and E-cadherin was predominantly localized in the membrane. However
cell contact became loose and E-cadherin was almost translocated to the cytoplasm in the tamoxifen-resistant MCF-7R cells. The migration was enhanced and the expression of vimentin and fibronectin was increased when the MCF-7 cells acquired tamoxifen resistance (P0.05). PI3K-Akt and MAPK/Erk signaling pathways were abnormally activated in the tamoxifen-resistant MCF-7R cells. Meanwhile
the migration and the expression of mesenchymal marker proteins were significantly suppressed when inhibiting PI3K-Akt pathway rather than MAPK/Erk pathway (P0.05). Conclusion EMT may contribute to the increased migration of tamoxifen-resistant breast cancer cells.