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Re-expression of miR-21 contributes to migration and invasion by inducing epithelial-mesenchymal transition consistent with cancer stem cell characteristics in MCF-7 cells
- 作者:Mingli Han (12)
Manran Liu (2) Yimeng Wang (3) Zhiqiang Mo (1) Xiaokai Bi (1) Zhirong Liu (1) Yuanming Fan (1) Xin Chen (1) chenxin1192@126.com Chengyi Wu (1) wuchengyi1192@163.com - 关键词:miR ; 21 8211 ; Epithelial ; mesenchymal transition 8211 ; Cancer stem cell 8211 ; Migration 8211 ; Invasion 8211 ; Breast cancer
- 刊名:Molecular and Cellular Biochemistry
- 出版年:2012
- 出版时间:April 2012
- 年:2012
- 卷:363
- 期:1-2
- 页码:427-436
- 全文大小:673.7 KB
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Department of Endocrine Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016 China2. The Key Laboratory of Laboratory Medical Diagnostics in the Ministry of Education and Department of Clinical Biochemistry, Chongqing Medical University, Chongqing, 400016 China3. Department of Emergency, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016 China
- 刊物类别:Biomedical and Life Sciences
- 刊物主题:Life Sciences
Biochemistry Medical Biochemistry Oncology Cardiology
- 出版者:Springer Netherlands
- ISSN:1573-4919
文摘
MiR-21 is known to play an important role in the development and progression, including migration and invasion, of many malignancies including breast cancer. Accumulating evidence suggest that the induction of epithelial8211;mesenchymal transition (EMT) phenotype and acquisition of cancer stem cell (CSC) characteristics are highly interrelated, and contribute to tumorigenesis, tumor progression, metastasis, and relapse. The molecular mechanisms underlying EMT and CSC characteristics during miR-21 contributes to cell migration and invasion of breast cancer are poorly understood. Therefore, we established miR-21 re-expressing breast cancer MCF-7 (MCF-7/miR-21) cells, which showed increasing cell growth, migration and invasion, self-renewal and clonogenicity. Our data showed that re-expression of miR-21 induced the acquisition of EMT phenotype by activation of mesenchymal cell markers (N-cadherin, Vimentin, α-SMA) and inhibition of epithelial cell marker (E-cadherin) in MCF-7/miR-21 cells, which consistent with increased cell subpopulation expressing CSC surface markers (ALDH1+ and CD44+/CD24−/low) and the capacity of sphereforming (mammospheres). Our results demonstrated that re-expression of miR-21 is responsible for migration and invasion by activating the EMT process and enhancing the characteristics of CSCs in MCF-7 cells.
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