Identification of epithelial-mesenchymal transition phenotype in tamoxifen-resistant MCF-7 cells

袁杰; 杨丽; 陈茂山; 朱庆; 付伟杰; 成宏; 柳满然; 杨光伦

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Identification of epithelial-mesenchymal transition phenotype in tamoxifen-resistant MCF-7 cells

更新时间：2026-01-09

- Identification of epithelial-mesenchymal transition phenotype in tamoxifen-resistant MCF-7 cells
- Journal of Army Medical University Vol. 36, Issue 22, Pages: 2272-2276(2014)
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  CLC： R394-33;R730.23;R737.9
- Published：2014
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袁杰,杨丽,陈茂山,朱庆,付伟杰,成宏,柳满然,杨光伦.人乳腺癌MCF-7他莫昔芬耐受细胞株EMT表型的鉴定及其机制的初步研究[J].陆军军医大学学报(原第三军医大学学报),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.
袁杰,杨丽,陈茂山,朱庆,付伟杰,成宏,柳满然,杨光伦.人乳腺癌MCF-7他莫昔芬耐受细胞株EMT表型的鉴定及其机制的初步研究[J].陆军军医大学学报(原第三军医大学学报),2014,36(22):2272-2276. DOI：

　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：

摘要

目的观察乳腺癌细胞MCF-7发生他莫昔芬耐受后细胞形态的变化及上皮-间质转化（epithelial-mesenchymal transition，EMT）现象，并初步研究其机制。方法免疫荧光染色观察乳腺癌细胞MCF-7及其他莫昔芬耐药株MCF-7R细胞的形态；qRT-PCR、Western blot检测两种细胞EMT相关标志蛋白的表达；Transwell法检测两种细胞的迁移能力；分别抑制PI3K-Akt及MAPK/Erk信号通路，检测MCF-7R细胞的迁移能力及EMT表型的变化。结果 MCF-7细胞间的联系紧密，发生他莫昔芬耐受后，细胞间隙明显增大；MCF-7细胞发生他莫昔芬耐受后迁移能力明显增强，并发现E-钙粘素(E-cadherin)分布从细胞膜向细胞质转移，波形蛋白（vimentin）及纤维粘连蛋白（fibronectin）表达水平明显升高（P0.05）；在耐药细胞中PI3K-Akt及MAPK/Erk信号通路均处于异常活化状态，抑制PI3K-Akt信号通路能明显抑制细胞的迁移能力，同时能使波形蛋白和纤维粘连蛋白表达水平降低（P0.05）。结论乳腺癌MCF-7细胞发生他莫昔芬耐受后其迁移能力增强可能与其发生EMT样表型有关。

Abstract

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.

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