[1]袁杰,杨丽,陈茂山,等.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,et al.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.
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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(/HTML )
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陆军军医大学学报(原第三军医大学学报)[ISSN:1000-5404/CN:51-1095/R]

卷:
36卷
期数:
2014年第22期
页码:
2272-2276
栏目:
论著
出版日期:
2014-11-30

文章信息/Info

Title:
Identification of epithelial-mesenchymal transition phenotype in tamoxifen-resistant MCF-7 cells
作者:
袁杰杨丽陈茂山朱庆付伟杰成宏柳满然杨光伦
重庆医科大学:附属第一医院内分泌乳腺外科,临床检验诊断学教育部重点实验室; 恩施土家族苗族自治州中心医院乳腺外科
Author(s):
Yuan Jie Yang Li Chen Maoshan Zhu Qing Fu Weijie Cheng Hong Liu Manran Yang Guanglun

Department of Endocriology and Breast Surgery, the First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016;Key Laboratory of Laboratory Medical Diagnosis of Ministry of Education, Chongqing Medical University, Chongqing, 400016; Department of Breast Surgery, Central Hospital of Enshi Autonomous Prefecture, Enshi, Hubei Province, 445000, China

关键词:
乳腺癌他莫昔芬耐受上皮-间质转化细胞迁移
Keywords:
breast cancer tamoxifen resistance epithelial-mesenchymal transition cell migration
分类号:
R394-33;R730.23;R737.9
文献标志码:
A
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(P<0.05);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(P<0.05)。      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 (P<0.05). 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 (P<0.05).       Conclusion      EMT may contribute to the increased migration of tamoxifen-resistant breast cancer cells.

相似文献/References:

[1]朱庆,伍俊仪,袁杰,等.新型雌激素受体GPER在乳腺癌MCF-7细胞他莫昔芬耐药中的作用及机制[J].陆军军医大学学报(原第三军医大学学报),2015,37(22):2249.
 Zhu Qing,Wu Junyi,Yuan Jie,et al.Role of G protein-coupled estrogen receptor in tamoxifen-resistant breast cancer MCF-7 cells[J].J Amry Med Univ (J Third Mil Med Univ),2015,37(22):2249.
[2]付伟杰,杨光伦,涂刚,等.S100p促进乳腺癌MCF-7细胞他莫西芬耐受和细胞迁移[J].陆军军医大学学报(原第三军医大学学报),2014,36(17):1795.
 Fu Weijie,Yang Guanglun,Tu Gang,et al.S100p promotes tamoxifen resistance and migration in human breast cancer MCF-7 cells[J].J Amry Med Univ (J Third Mil Med Univ),2014,36(22):1795.

更新日期/Last Update: 2014-11-18